This chapter examines the epidemiologic studies on the relationship between adverse long-term health outcomes and exposure to combustion products thought by the committee to be comparable to those emitted from the military burn pits in Iraq and Afghanistan. The media has described disheartening stories of returning Iraq and Afghanistan veterans with unusual and often multiple medical problems, anecdotally associated with exposure to smoke from burn pits. Stories published in the New York Times and Washington Post (both on August 6, 2010) describe individuals with disabling respiratory diseases, reports of constrictive bronchiolitis (an unusual lung disease), leukemia, and other cancers, and a claim of increased rates of asthma, all suggested to be linked to exposures to burn pits (Glod 2010; Risen 2010). However, such anecdotal reports do not demonstrate causality or even association; the committee looked instead to the epidemiologic literature on the exposed populations, and on populations similarly exposed. This chapter describes the committee’s approach to reviewing the literature, the main uncertainties and limitations associated with the studies, summarizes the Department of Defense’s (DoD’s) report of several epidemiologic studies particular to health effects and burn pit exposure, summarizes the available literature by health outcome, and presents the committee’s conclusions.
APPROACH TO THE EPIDEMIOLOGIC LITERATURE
Chapters 4 and 5 identified specific contaminants present at Joint Base Balad (JBB) and outlined their potential human health effects. These health effects are, in many cases, based on animal studies, and usually only pertain to exposure to a single chemical, not mixtures of chemicals from burning materials. Thus, the committee thought it necessary to evaluate human health effects to the complex mixture of chemicals resulting from combustion. The committee began by reviewing health studies on military personnel exposed to burn pits in Iraq and Afghanistan. As discussed in Chapter 3, however, there are few such studies available. Thus, the committee decided to approach its review of the health effects stemming from exposure to burn pits by identifying populations that were considered to be the most similar to military personnel with regard to exposures to burn pits or other sources of combustion products. The committee then conducted an extensive literature search for epidemiologic studies on long-term health outcomes seen in those populations. Pertinent studies were reviewed and classified as “key” or “supporting” based on their quality and relevance to the task. These key and supporting studies formed the basis of the committee’s weight-of-the-evidence approach and its conclusions on the degree of association demonstrated between exposure to combustion products and long-term health outcomes. In the following sections, the com-
mittee discusses the selection and characteristics of the surrogate populations, the methods used for the literature searches, the criteria to distinguish key and supporting studies, and the categories of association on which the committee’s conclusions were based.
Populations of Interest
The committee reviewed and evaluated the epidemiologic literature for studies on populations with inhalation exposure to chemical mixtures that were considered to be similar to burn pit emissions, that is, mixtures formed by combustion of a variety of materials and waste in occupational and environmental exposure settings. Two occupational groups were identified as most likely to have comparable exposures: firefighters, including those with exposures to wildland and chemical fires, and incinerator workers. Firefighters are exposed to highly complex chemical mixtures (McGregor 2005; IARC 2010). The short intermittent spikes in exposure for firefighters are likely to differ from the long-term, chronic exposures to burn pit emissions on military bases; nevertheless, studies on firefighters are useful as the best available representation of exposures to mixtures of combustion products.
The waste disposed in burn pits is described by the DoD as municipal waste (Taylor et al. 2008). Therefore, occupational exposures to emissions from municipal incinerators were considered to be another surrogate for exposure of military personnel to burn pit emissions. Furthermore, because military personnel at JBB and other burn pit locations not only work on the base but also live there, the committee considered the literature on the health effects seen in residents living near municipal incinerators to be of interest. The committee acknowledges that exposures to emissions from municipal waste incinerators likely differ from exposures to burn pit emissions, and the value of these studies in understanding the health effects of burn pit exposures is limited.
Studies of military personnel exposed to smoke from oil-well fires in Kuwait during the 1990–1991 Gulf War were also considered. Assessments of health effects among Gulf War veterans are particularly useful because of the common background exposures (for example, dusty environment, vehicle exhaust, munitions) and personnel characteristics (for example, underlying health, exposure to stressors, general demographics) shared by those deployed to Operation Enduring Freedom (OEF) in Afghanistan and Operation Iraqi Freedom (OIF) in Iraq.
The committee acknowledges that its ability to compare exposures among the populations of interest is restricted by the unknown degree to which exposures of varying intensity, duration (short-term, intermittent exposure to combustion products for firefighters; chronic exposures for incinerator workers and those living near incinerators; short-term exposure to oil-well–fire smoke in Kuwait), and composition can be extrapolated to the burn pit exposure of military personnel at JBB and elsewhere. Military personnel at JBB might have been exposed for a few days or up to 12 months as they lived and worked on the base whereas firefighters and incinerator workers might experience occupational exposure for many years, and residents near incinerators might be subject to a lifetime of exposure to pollutants. The committee recognized that JBB personnel may have had days of high exposures when smoke and emissions from the burn pits spread across the camp, but on other days there may have been less smoke, and the overall level of emissions was unknown. Exposure to burn pit emissions via ingestion and dermal contact is an even greater unknown as no sampling of surfaces and soil was conducted. Exposure to combustion products among all groups is likely affected by time-dependent changes in engineering or other controls. For example, some firefighter studies cited in this chapter were conducted before the use of self-contained breathing apparatus and other protective gear was common, while other studies assessed firefighters using protective gear that minimized exposure. The same is true for occupational and environment exposure to incinerator emissions; engineering controls to minimize hazardous emissions have been implemented over time. At JBB, the composition and volume of the burn pit changed as practices to separate waste and the use of incinerators were implemented. Since the composition of combustion products varies greatly depending on burn characteristics and fuel, and little is known about specific exposures to the burn pits at JBB and elsewhere, the committee was unable to directly compare constituents and concentrations of the pollutants that military personnel at JBB and the surrogate populations were exposed to, nor was it able to compare the duration and frequency of these exposures.
Furthermore, all the groups considered in this chapter experience a variety of additional exposures independent of their exposure to combustion products from burn pits, fires, or municipal incinerator emissions. These additional exposures include emissions from diesel engines (aircraft, vehicular, and machinery), kerosene heaters, and other
environmental stressors such as combat exposure, job-related stress, and other environmental pollutants such as dust storms. The committee focused on health effects related to combustion products as related to burn pits and did not attempt to assess health effects from these other exposures.
The committee did not consider studies of health effects reported for first responders to the World Trade Center attacks in 2001 because the composition of the smoke and emissions from this event are substantially different from combustion emissions, particularly those expected from burn pits.
Extensive searches of the scientific literature published after 1980 were conducted using two major biomedical databases: MEDLINE and EMBASE. The literature search for long-term health effects among firefighters retrieved over 400 studies, including studies of structural fires, wildland or forest fires, and chemical fires. The titles and abstracts of those studies were reviewed and studies that did not appear to be immediately relevant were deleted from the database. Deleted studies included those not linked to inhalation exposure (such as studies of job-related stress); studies that had fewer than 10 participants; studies of acute or short-term health effects only (unless considered relevant to long-term effects); studies of exposures to uranium and other types of radiation; studies reporting behavioral or psychiatric outcomes; or studies that assessed DNA or other cellular damage. The literature search for incineration workers and residents of nearby communities also returned over 400 studies. In this case, rejected studies included those that were not linked to inhalation exposures; studies that reported acute or short-term health effects only; studies that were modeling studies of emissions or that focused on children, genetics, or DNA damage; and studies of ambient air pollution. Studies that characterized emissions from incinerators but not their health effects, or that focused on waste management, were also rejected.
The committee adopted a policy of using only published papers that had undergone peer review as the basis of its conclusions. An exception was made for the epidemiologic studies conducted by the DoD to assess health effects in military personnel exposed to burn pits; theses studies are summarized below and discussed after the peer reviewed epidemiologic studies for each health outcome. Since epidemiologic studies of Gulf War veterans have been described previously by other Institute of Medicine (IOM) committees, most recently in Volume 8 of the Gulf War and Health series (IOM 2010), this committee relied on those assessments supplemented with a review of more recent publications.
Key and Supporting Studies
After the removal of the extraneous studies, the full text of the remaining articles and reports were retrieved. For each health outcome, committee members reviewed the studies most closely related to their area of expertise, to determine whether the criteria for a key or supporting study were met. Consistent with previous IOM reports (IOM 2010), to be designated as key, a study had to be published in a peer-reviewed journal, present information about the putative exposure and specific health outcomes, demonstrate rigorous methods, include methodological details adequate to allow a thorough assessment, and use an appropriate control or reference group. A supporting study typically had methodological limitations, such as lack of a rigorous or well-defined diagnostic method or a lack of an appropriate control group. The committee as a group reviewed the key and supporting studies identified by the committee members responsible for each health outcome. The strengths and limitations of each study and its categorization as key or supporting were discussed in plenary session and a consensus reached on its contribution to the evidence base for each category of association for each health outcome. After having reviewed all the studies in detail, the committee based its conclusions primarily on key studies. Supporting studies are included as part of the committee’s analysis because they provide information that might modify confidence in the conclusions based on key studies, but they carry less weight than key studies. The committee considered the DoD epidemiologic studies as supporting literature when making conclusions about associations between exposure to combustion products and health outcomes.
Categories of Association
For its conclusions, the committee agreed to use the categories of association that have been established and used by previous IOM committees, such as those that prepared the Veterans and Agent Orange reports and the Gulf War and Health series. These categories of association have been accepted for more than a decade by Congress, the Department of Veterans Affairs (VA) and the DoD, researchers, and veterans’ groups.
The five categories describe different levels of association;1 the validity of an association is likely to vary to the extent to which common sources of spurious associations could be ruled out as the reason for the observed association. Accordingly, the criteria for each category express a degree of confidence based on the extent to which sources of error and bias were reduced. The committee discussed the evidence and reached consensus on the categorization of the evidence for each health outcome in this chapter. The committee used the following categories:
- Sufficient Evidence of a Causal Relationship: Evidence is sufficient to conclude that a causal relationship exists between exposure to combustion products and a health outcome in humans. The evidence fulfills the criteria for sufficient evidence of a causal association and satisfies several of the criteria used to assess causality: strength of association, dose–response relationship, consistency of association, temporal relationship, specificity of association, and biologic plausibility.
- Sufficient Evidence of an Association: Evidence is sufficient to conclude that there is a positive association. That is, a positive association has been observed between exposure to combustion products and a health outcome in human studies in which bias and confounding could be ruled out with reasonable confidence.
- Limited/Suggestive Evidence of an Association: Evidence is suggestive of an association between exposure to combustion products and a health outcome in humans, but this is limited because chance, bias, and confounding could not be ruled out with confidence.
- Inadequate/Insufficient Evidence to Determine Whether an Association Does or Does Not Exist: The available studies are of insufficient quality, consistency, or statistical power to permit a conclusion regarding the presence or absence of an association between exposure to combustion products and a health outcome in humans.
- Limited/Suggestive Evidence of No Association: There are several adequate studies, covering the full range of levels of exposure that humans are known to encounter, that are mutually consistent in not showing a positive association between exposure to combustion products and a health outcome. A conclusion of no association is inevitably limited to the conditions, levels of exposure, and length of observation covered by the available studies. In addition, the possibility of a very small increase in risk at the levels of exposure studied can never be excluded.
UNCERTAINTY AND LIMITATIONS OF THE STUDIES
The studies cited in this chapter have limitations and uncertainties, some common to epidemiologic studies in general, and some specific to studies of occupational populations. These limitations and uncertainties include
- Healthy worker effect—Studies of firefighters are likely to be biased downward when the comparison group is the general population, that is, risk estimates might reflect a lower risk than really exists because firefighters must meet physical health standards for employment, and must remain healthy to continue working. Thus, firefighters might have a better health status than members of the general population of the same sex and age.
- Exposure misclassification—None of the studies cited in this chapter have actual measures of inhalation to combustion products. Without measured individual exposure information, an individual might be assigned the wrong level of exposure thus masking the association between effect and exposure. Most studies use employment as a firefighter (yes/no) as the only measure of exposure, although a few studies used additional
1The following categories of association are excerpted from Gulf War and Health: Volume 1 (IOM 2000).
measures to better define exposures, such as the number of years employed or number of fires attended. Studies of communities in the vicinity of an incinerator rely on distance from the incinerator as the best surrogate of residential exposure, using either classification into concentric rings around the site or modeled exposure estimates. Ecological study designs are limited to using information on residential history, which can lead to exposure misclassification. Not all studies report the type of waste being burned, the age or technological practices of the incinerator, or adherence to government regulations, all of which affect the amount and constituents of the emissions. Furthermore, communities might be affected by other pollution sources, such as local industry, so that exposure to an environmental contaminant cannot be wholly attributed to the incinerator.
- Lack of information on confounders—Most of the studies do not adjust for potential confounders such as tobacco smoking and alcohol consumption. The use of tobacco products, particularly cigarettes, has been causally associated with long-term adverse health effects (U.S. Surgeon General 1964). Military personnel have a greater prevalence of tobacco use than civilians, particularly when deployed where smoking rates might be as high as 50% (IOM 2009). Tobacco smoke contains many environmental contaminants, including particulate matter (PM), acrolein, polyaromatic hydrocarbons (PAHs), benzene, and metals. The 2004 U.S. Surgeon General’s report associated tobacco smoke with cancer, cardiovascular disease (CVD), pulmonary disease, gastrointestinal disease, and reproductive effects (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 CVD (IOM 2010).
- Limited statistical power—Small sample size in many of the studies prevents the detection of associations for the less common health outcomes such as rare cancers.
- Disease misclassification—Many of the studies in this chapter investigate mortality based on the cause of death listed on death certificates. The validity of these mortality studies is dependent on the accuracy of the reported cause of death.
- Publication bias—It is likely that the evidence base for some health outcomes is affected by publication bias, that is, results that are positive or statistically significant are more likely to be published than null results.
The variability of the studies’ results and methods makes comparison across them difficult. Variables include different criteria for reference populations, lack of adjustment for confounding factors, and different statistical methods. In addition, there is uncertainty regarding the degree of similarity between the exposures to combustion products in the studies and exposure to the emissions from the burn pits. Despite these limitations, the studies reviewed in this chapter provide useful evidence on the potential health effects that might be associated with exposure to burn pits. They also highlight the many challenges inherent in the conduct of any epidemiologic study of exposure to complex mixtures.
Health outcomes were investigated by organ system. The committee drew conclusions for the following health outcomes: respiratory, circulatory, neurologic, reproductive and developmental effects, and cancer. In addition, the committee examined the literature on other outcomes such as the autoimmune disorders systemic lupus erythematosus and rheumatoid arthritis, and on chronic multisymptom illness because these health outcomes were evaluated in the DoD epidemiologic studies of OEF/OIF military personnel deployed to sites with burn pits (AFHSC et al. 2010).
Results from the epidemiologic literature are reported here for each health outcome and organized by population (firefighters, incinerator workers and surrounding communities, and Gulf War veterans exposed to smoke from oil-well fires). Little information is available on health effects linked directly to burn pit exposure; however, two epidemiologic studies conducted by the Armed Forces Surveillance Center, Naval Health Research Center (NHRC), and U.S. Army Public Health Command (AFHSC et al. 2010) on health outcomes among OEF/OIF troops deployed to bases with burn pits are considered. A brief discussion of the key and supporting studies and a
conclusion are provided for each health outcome. The committee assigns a category of association for each health outcome after a summary of the results.
For readers interested in more details for the key and supporting studies, descriptions of the study design, population, exposures, outcomes measured, adjustments, and limitations are given in tabular format in Appendix C in alphabetical order by study author rather than by health outcome to avoid duplication of studies reporting on multiple outcomes.
DoD Epidemiologic Investigations
In May 2010, the Armed Forces Health Surveillance Center (AFHSC), the Naval Health Research Center (NHRC), and the U.S. Army Public Health Command (APHC) released a report on five epidemiologic studies of military personnel deployed to burn pit sites in Iraq (AFHSC et al. 2010). In the studies, exposure was defined as deployment to a site with an active burn pit as individual exposure data were not available. The AFHSC retrospective cohort study compared the incidence rates of various diseases, among deployed (two locations with burn pits, two locations without burn pits, and Korea) and never deployed cohorts. The cohorts consisted of Army and Air Force personnel deployed between January 1, 2005, and June 30, 2007, to one of four U.S. Central Command (CENTCOM) bases or to the Republic of Korea. CENTCOM bases were Joint Base Balad (JBB) and Camp Taji in Iraq, both of which had burn pits, and Camp Buehring and Camp Arifan in Kuwait which did not have burn pits. Active-duty personnel who were located within a 3-mile radius of a burn pit were included in the exposed groups. There were 15,908 personnel who served at JBB; 2,522 personnel at Taji; and 51,299 personnel at bases without burn pits. Military personnel were included in the study if they served at least 31 days at a base by the end of their deployment in order to capture any health effects resulting from being at the base. Camps in the Republic of Korea had no burn pits but were subject to urban air pollution and PM from the surrounding desert. The comparison group consisted of 237,714 active-duty personnel stationed in the United States and not previously deployed. All individuals were followed from their return from deployment, or April 15, 2006, and censored at the earliest occurrence of a diagnosis of interest, separation from active service, start of subsequent deployment or change of station, or the end of the 36-month follow-up period. The analysis adjusted for age, race, grade, and service. The report included several different investigations: (1) incidence rates of respiratory conditions, circulatory disease, CVD, sleep apnea, and ill-defined conditions for deployed personnel versus nondeployed personnel; (2) responses to post-deployment health surveys were compared between deployed personnel at sites with or without active burn pits; and (3) medical encounters for respiratory outcomes were compared for deployed personnel at sites with or without burn pits. The investigation of medical encounters while deployed is not discussed in this chapter because such encounters were considered to relate to acute, rather than long-term, health effects (AFHSC et al. 2010).
This AFHSC study looked only at health effects occurring within 36 months after return from a site with an active burn pit. Follow-up was not long enough to detect diseases with long latency, such as cancer. There was no adjustment for confounders such as smoking. This study had a large population and was able to capture individuals’ health status using electronic medical records. The DoD concluded that, based on in-theater reports of respiratory problems and the high proportion of Air Force personnel reporting exposure to burn pits at JBB, acute respiratory effects are of concern, and possible long-term health effects are not discussed in the report (AFHSC et al. 2010).
The DoD report also contains four NHRC studies that looked at the personnel stationed at the same bases as for the AFHSC study but the NHRC also included a third base in Iraq with a burn pit, Camp Speicher. Exposure was based on being located within a 5-mile radius of a documented burn pit. The first study assessed birth outcomes in infants of military personnel exposed before or during pregnancy to burn pits and is discussed in the section of this chapter on reproductive and developmental outcomes. The second study looked at respiratory health of military personnel who had been exposed to burn pits and were participants in the Millennium Cohort Study; this study is discussed in the section of this chapter on respiratory outcomes. The third and fourth studies, also of participants of the Millennium Cohort Study, focused on service members who had been exposed to burn pits and their risk of having chronic multisymptom illness (CMI), or of having physician-diagnosed lupus or rheumatoid arthritis, respectively. The Millennium Cohort examined by NHRC consisted of more than 27,000 personnel deployed in support of OEF/OIF and included over 3,000 participants considered exposed, with at least one deployment
within a 5-mile radius of a documented burn pit. Exposed participants were compared with participants who were deployed to locations without burn pits. The Millennium Cohort is considered to represent U.S. military personnel, with reliable self-reported information obtained prior to enrollment and unaffected by subsequent health status.
CMI was defined by the reporting of at least two symptoms from the following categories: general fatigue, mood and cognition, and musculoskeletal. CMI was not significantly associated (p = 0.16) with being deployed within a 5-mile radius of a burn pit, cumulative exposure to a burn pit overall, or being deployed to JBB or Camps Taji or Speicher, when adjusted for sex, birth year, education, service component, service branch, pay grade, smoking status, alcohol-related problems, mental health symptoms, and baseline CMI status. However, cumulative exposure to a burn pit for more than 210 days showed a slight increase in risk for CMI (OR 1.22, 95% CI 1.04–1.44) after adjustment.
There was no association between a new diagnosis of lupus and being within 5 miles of a burn pit, cumulative exposure, or being deployed to Camp Taji or Camp Speicher. There was, however, a significant increase in the likelihood of a lupus diagnosis for those deployed to JBB (OR 3.52, 95% CI 1.59–7.79) compared with those deployed to locations without burn pits. For rheumatoid arthritis, there was no association with deployment to a burn pit location, cumulative days exposed, or camp site. One exception was an increase in rheumatoid arthritis diagnoses for those exposed to burn pits for 132–211 days (OR 2.03, 95% CI 1.18–3.49), although exposure for more than 211 days was not significant. Electronic medical records were used to confirm 33% of self-reported lupus cases and 17% of self-reported rheumatoid arthritis cases among active-duty personnel diagnosed while in the military. Among verified cases, no association between lupus or rheumatoid arthritis and exposure to burn pits was found (AFHSC et al. 2010).
There are several limitations to using the Millennium Cohort data. Confirmation of self-reported medical issues is difficult for participants who are not active-duty allowing for disease misclassification. The rare occurrences of bronchitis, emphysema, lupus, and rheumatoid arthritis and short average follow-up (2.8 years) compromise the precision of the risk estimates (AFHSC et al. 2010). Exposure misclassification is also possible as individual exposure information was not available.
The committee categorized these DoD studies as supporting due to the short period of follow-up (36 months), ecologic nature, lack of information on other hazardous environmental exposures common in the context of desert and war (for example, smoking, diesel exhaust, kerosene heaters, PM, local and regional pollution). However, as the only studies of health effects and burn pit exposure, they are uniquely valuable to the current assessment and provide the first indications of adverse health effects resulting from exposure to burn pits. The lack of additional studies and further followup to corroborate or refute the DoD’s reported findings prevent the committee from being able to make decisions about the strength of an association between burn pits and the reported health outcomes.
DISEASES OF THE RESPIRATORY SYSTEM
Environmental conditions experienced by military personnel in Iraq and Afghanistan might cause respiratory effects from exposure to windblown dust, local combustion sources, and volatile evaporative emissions. The local combustion sources include burn pits or other waste incinerators, compression ignition vehicles, aircraft engines, diesel electric generators, and local industry and households. Although local contributions of wood smoke might be minimal (there is mention in the sampling field notes of a local brush fire causing smoky conditions), exposure to wood smoke from burn pits would have been likely (burning of materials such as shipping pallets). Asthma, bronchitis, chronic obstructive pulmonary disease (COPD), and respiratory symptoms have been reported to occur more frequently than expected among Gulf War veterans (IOM 2010). A retrospective case-control study found a higher risk of new-onset asthma (OR 1.58, 95% CI 1.18–2.11) among military personnel who served in OEF/OIF, compared with age- and sex-matched personnel deployed in the United States (Szema 2010). Personnel exposed to combustion products from burn pits might be at increased risk of respiratory diseases as some chemicals released by the burning of waste (as described in Chapters 4 and 5), such as acrolein and PM, are known to cause respiratory effects (see Chapter 5).
This section focuses on long-term, nonmalignant adverse respiratory conditions resulting from exposures to combustion products that are considered to be similar to burn pit emissions. First, respiratory outcomes (assess-
ments of respiratory disease and pulmonary function indicative of potential disease) related to occupational exposures of firefighters (including firefighters involved in structural, wildland, and chemical fires) are considered. Next, respiratory outcomes from exposure to incinerators, both for workers and surrounding communities are discussed. Lastly, respiratory outcomes for veterans exposed to oil-well fires in the 1990–1991 Gulf War and the preliminary data available for veterans from OEF/OIF will be examined. Details of the studies presented in this section are found in Appendix C.
Respiratory Disease in Firefighters
The committee recognizes that firefighter exposures may be very different depending on the type of fire. Structural firefighters primarily work to extinguish fires on anthropogenic objects—for example, buildings, furniture, manufactured items—whereas wildland firefighters are exposed to combustion products from the burning of the natural environment, that is, forests and grasslands. Firefighters working to extinguish chemical fires might be exposed to a wide variety of combustion products as well as the unburned chemical(s) itself.
No key studies of respiratory diseases in firefighters were identified by the committee.
Fifteen studies were considered to be supportive. Of the 13 studies reporting on mortality, all reported no significant increase and even reductions in mortality from respiratory causes (Eliopulos et al. 1984; Feuer and Rosenman 1986; Vena and Fiedler 1987; Heyer et al. 1990; Rosenstock et al. 1990; Beaumont et al. 1991; Grimes et al. 1991; Demers et al. 1992a, 1995; Guidotti 1993; Aronson et al. 1994; Baris et al. 2001; Ma et al. 2005). In the largest study, Ma et al. (2005), found firefighters to have significantly lower mortality rates for all respiratory causes, and for pneumonia specifically, compared with the general Florida population. However, the 13 studies had one or more limitations that precluded their categorization as key studies including too few deaths for meaningful statistical analyses, exposure assessments that were dichotomous (employed as a firefighter, Y/N) or absent, and failure to consider tobacco smoking or the healthy worker effect.
There is concern that environmental exposures could contribute to respiratory diseases of unknown cause such as sarcoidosis. Sarcoidosis is a systemic disease characterized by granulomatous inflammation, most often involving lymph nodes and the lung, but also involving the eyes, skin, liver, heart, and central nervous system. Prezant et al. (1999) studied the annual incidence and point prevalence of biopsy-proven sarcoidosis in New York City firefighters and emergency medical personnel between 1985 and 1988. The average annual incidence among firefighters was 12.9 cases per 100,000 firefighters and the point prevalence in 1998 was 222 cases per 100,000 firefighters. The majority of those with sarcoidosis (23 of 25) had minimal impairment as assessed by radiograph (x-ray and CT scan) and pulmonary function testing. These data suggest an association between firefighting and sarcoidosis, but confirmatory studies are lacking and causation was not demonstrated.
There are few studies on the health consequences of fighting chemical fires. One longitudinal follow-up study of firefighters exposed to a 1985 fire burning polyvinyl chloride found that exposed firefighters had significantly more respiratory symptoms (cough, wheeze, shortness of breath, chest pains) at both 5–6 weeks and 22 months postexposure than unexposed firefighters with the exception of wheezing at 22 months (Markowitz 1989). Among exposed firefighters, the incidence of respiratory symptoms showed a decreasing trend over time and respiratory scores between the two time points were well correlated. The findings were similar among current, past, and never smokers. After 22 months, 12 of 64 (18%) of exposed firefighters had been diagnosed with asthma or bronchitis by a physician whereas none of the 22 controls had these diagnoses. This study is limited to a single heavy exposure to a specific set of chemicals.
Pulmonary Function in Firefighters
Pulmonary function tests are frequently used to diagnose respiratory diseases such as asthma, bronchitis, emphysema, or fibrosis. Measurements include spirometry (the flow rate and volume of air that is inhaled or exhaled), diffusion capacity (how well oxygen moves from the lungs into the blood), and lung volumes (the total amount of air in the lungs). Testing might be used to evaluate shortness of breath, diagnose disease, and track disease progression or effects of treatments/medicines (Medline Plus 2011). Pulmonary function effects can be observed even in the absence of clinical symptoms or disease.
Sparrow et al. (1982) conducted a longitudinal study of pulmonary function in 168 male firefighters who were participants in the larger Normative Aging Study of 2,280 male military veterans that began in 1963 in Boston. Spirometric measurements, as well as a survey of smoking habits and respiratory symptoms, were collected at 5-year intervals. The control group was a non-firefighting population from the same study. The authors found a significantly greater loss of forced vital capacity (FVC) and forced expiratory volume in one second (FEV1) in the firefighters even after adjusting for smoking, age, height, and initial pulmonary function level (p < 0.05). Few respiratory symptoms and diseases were reported during follow-up, with no differences between firefighters and controls.
Peters et al. (1974) studied pulmonary function in 1,430 Boston firefighters. Repeat pulmonary function tests and questionnaires collecting self-reported respiratory symptoms and smoking habits were completed from 1970 to 1972. Pulmonary function declined in the entire cohort (FVC annual loss of 77 mL, FEV1 of 68 mL) and was significantly associated with frequency of exposure to fires (p < 0.01). Decreases could not be explained by the effects of age, smoking, or race. Additional follow-up of 1,146 firefighters through 1974 showed that decreased pulmonary function and association with numbers of fires fought was maintained (Musk et al. 1978). However, a further follow-up of this cohort for a total of 6 years through 1976, found smaller declines in FVC and FEV1, no correlation with exposure, and no significant difference from healthy nonsmoking non-firefighters (Musk et al. 1982). This change was attributed to increased use of protective respiratory equipment.
Supporting studies of pulmonary function show mixed results. Several studies report no decrease in pulmonary function for firefighters while other studies indicate increases in respiratory symptoms. Decreased pulmonary function was reported for structural firefighters (Unger et al. 1980; Tepper et al. 1991) and for forest firefighters (Liu et al. 1992; Serra et al. 1996; Betchley et al. 1997).
An examination of respiratory function among 128 firefighters and 88 controls in Zagreb, Croatia, found significantly higher rates (p < 0.01) of respiratory symptoms (dyspnea, nasal catarrh, sinusitis, and hoarseness) and decreased pulmonary function in firefighters compared to controls (Mustajbegovic et al. 2001). The authors found these chronic respiratory symptoms and decreases in pulmonary function to be associated with duration of employment and smoking. Young et al. (1980) conducted a cross-sectional study of respiratory disease and pulmonary function among 193 firefighters in New South Wales, Australia. The authors found no increased respiratory problems attributable to fire exposure and concluded that “the major combustion products responsible for respiratory damage were self-administered, arising from burning tobacco rather than from burning buildings.” Miedinger et al. (2007) examined respiratory symptoms, atopy, and bronchial hyperreactivity in 101 professional firefighters compared with 735 local men in Basel, Switzerland. Firefighters had better FEV1, FVC (significant), and FEV1/FVC values than controls, although they also had elevated rates of respiratory symptoms, atopy, and bronchial hyperreactivity (OR 2.24, 95% CI 1.12–4.48). Douglas et al. (1985) examined the effect of firefighting on the pulmonary function of 1,006 London firefighters over 1 year. Lower than expected pulmonary function was not associated with exposure, based on years of employment and self-reported exposure to severe smoke
events, except for a nonsignificant decrease among firemen who had worked for more than 20 years. This analysis adjusted for smoking.
Horsfield et al. (1988a,b) conducted two longitudinal studies of respiratory health in 96 West Sussex firefighters and 69 local nonsmoking men assessed every six months for 2 years and annually thereafter over the course of 4 years. Respiratory symptoms increased at a faster rate for firemen, regardless of smoking status, compared with the nonsmoking controls, leading the authors to conclude “these results suggest that being affected by smoke and fumes at work may be a cause of long-term symptoms in firemen” (Horsfield et al. 1988b). However, the control group had a greater decrease in pulmonary function and spirometric measurements than the firemen, leading the authors to further conclude that “these results show no evidence of chronic lung damage in West Sussex firemen” (Horsfield et al. 1988a). They attributed these findings not only to a healthy-worker selection bias but to the increasing use of protective breathing apparatus by these firemen.
Unger (1980) investigated the acute and chronic effects of a severe smoke exposure event on the pulmonary function of 30 firefighters sent to a Houston-area hospital after a single fire. Spirometric data and a survey of self-reported symptoms were collected immediately, after 6 weeks, and again after 18 months. Significant decreases in FVC (p < 0.01) and FEV1 (p < 0.05) were observed compared to matched controls. Tepper et al. (1991) evaluated pulmonary function changes after 6 to 10 years in male Baltimore firefighters (n = 632) in a longitudinal cohort study that adjusted for age, smoking, blood type, and weight. Firefighters who did not wear respirators and those who were exposed to ammonia were both found to have 1.7 times the rate of decrease in FEV1 of unexposed controls. Active firefighting was associated with 2.5 times (p < 0.05) the rate of decrease compared with individuals no longer working as firefighters.
Three studies investigated forest firefighters. Two examined cross-season differences in respiratory function. Liu et al. (1992) conducted a longitudinal study of 63 seasonal and full-time wildland firefighters in Northern California and Montana, pre- and post firefighting season in 1989. The authors found a postseasonal loss in lung function (0.15 L FEV1) and an increase in airway responsiveness (significant mean declines in FVC, FEV11, and FEF25–75) compared with preseason values after controlling for smoking. Betchley et al. (1997) observed significant decreases (p < 0.05) in cross-season spirometry values for 53 forest firefighters based on questionnaires and testing before and after the 1992 firefighting season. Mean individual decreases were 0.033 L for FVC1, 0.104 L for FEV1, and 0.275 L/sec for FEF25–75. The authors also reported significant decreases in pulmonary function across shifts for the 72 individuals assessed for cross-shift differences. Results were not affected by smoking, recent colds, lung conditions, allergies, or other potential confounders with the exception of those relying on wood to heat their homes. The third study of forest firefighters by Serra et al. (1996), examined pulmonary function in 92 Sardinian forest firefighters compared with 51 local police officers. The firefighters had significant decreases in FEV1, FVC, FEF75, FEV1/FVC, FEF50, FEF25, but the decreases were not correlated with length of service or number of fires extinguished after adjusting for age, height, smoking status, and pack-years. No difference in permeability of alveolar-capillary barrier was observed.
Respiratory Disease in Incinerator Workers
No studies of occupational respiratory disease among incinerator workers were identified by the committee.
Pulmonary Function in Incinerator Workers
No key studies of pulmonary function in incinerator workers were identified.
Three supporting studies of pulmonary function in incinerator workers were considered by the committee. Bresnitz et al. (1992) conducted a cross-sectional study of 89 male incinerator workers in Philadelphia, Pennsylvania. The study included environmental monitoring, physical examinations of all study participants, analysis of biological samples, and pulmonary function tests. The prevalence of pulmonary function patterns were similar in high and low exposed groups, after adjusting for smoking status. The OR for small airway obstruction in the high versus low exposed group was 1.19 (95% CI = 0.45–3.16). Changes in pulmonary function were related only to smoking status. Conversely, two other studies report decreased pulmonary function among incinerator workers after adjusting for smoking. Charbotel et al. (2005) noted significantly reduced pulmonary function from predicted values in the third year of monitoring—FEF50 (p = 0.04), FEF25–75 (p = 0.02) and FEF25–75/FVC (p = 0.01)—among 83 workers exposed to incinerator emissions compared with 76 unexposed workers, indicating possible obstructive disorders for the exposed workers. After adjusting for history of allergy or lung disease, smoking, and location of examination, the reduction of FEF75 in the first year and FEF25–75/FVC in the third year were linked to exposure in incinerator plants. Charbotel et al. (2005) noted that daily variation in lung function may not have been captured. A study of 102 male workers at three French urban incinerators by job type was conducted by Hours et al. (2003). Symptoms were self-reported on a survey and a physical exam was performed with blood testing and respiratory function assessment. Workers were compared with 84 water-meter assemblers, security guards, or woolen-mill workers. Daily coughing was reported more often by incinerator furnace men (OR = 6.58, 95% CI 2.18–19.85) and decreased respiratory performance was found in incinerator maintenance and effluent treatment workers (p < 0.01) after adjusting for smoking, age, and work location.
Respiratory Disease in Communities Near Incinerators
No studies assessing respiratory disease incidence or mortality in populations exposed to incinerator emissins were identified by the committee.
Pulmonary Function in Communities Near Incinerators
No key studies of pulmonary function in populations exposed to incinerator emissions were identified by the committee.
Four studies, conducted as part of the Health and Clean Air Study (Shy et al. 1995), assessed health outcomes in communities living near incinerators. Exposure was based on distance from an incinerator. No significant differences were noted between respiratory symptoms or pulmonary function and community exposure to incinerator emissions (Shy et al. 1995; Lee and Shy 1999; Hu et al. 2001; Hazucha et al. 2002). Using the Health and Clean Air Study (Shy et al. 1995) and one additional community near a commercial hazardous waste incinerator, Mohan et al. (2000) compared respiratory symptoms with four control communities matched by socioeconomic characteristics and population size. The authors found a higher prevalence of all respiratory symptoms in the one community near a hazardous waste incinerator compared with the control community (p < 0.05) even after controlling for perceptions of air quality.
Respiratory Disease in Gulf War Veterans Exposed to Oil-Well–Fire Smoke
Studies of respiratory outcomes related to exposure to smoke from oil-well fires were reviewed by previous IOM committees tasked with assessing long-term health effects in Gulf War veterans (IOM 2006). Those committees noted that these veteran studies are valuable for their relatively robust exposure estimates; however, the studies generally lack the temporal context to distinguish between new respiratory illness and pre-existing conditions (for example, asthma that was present before deployment versus asthma onset after exposure to oil-well fire smoke).
Gulf War and Health: Volume 4 (IOM 2006) identified three key studies,2 all using similar methods to describe troop exposure to smoke from oil-well fires by linking troop locations and National Oceanic and Atmospheric Administration (NOAA) meteorologic information, and to assess risks of respiratory diseases (Cowan 2002; Lange 2002; Smith 2002). Cowan et al. (2002) conducted a case-control study to identify cases of physician-diagnosed asthma in a DoD registry of clinically evaluated active-duty Gulf War Veterans (n = 873) and controls without asthma (n = 2,464). Self-reported oil-well–fire smoke exposure was associated with a higher risk of asthma (OR 1.56, 95% CI 1.23–1.97). In addition, modeled cumulative oil-well–fire smoke exposure was also related to a greater risk of asthma (OR 1.08, 95% CI 1.01–1.15) and showed the greatest risk among those with greater exposures (OR 1.21, 95% CI 0.97–1.51 for the intermediate-exposure group of up to 1.0 mg-day/m3; and OR 1.40, 95% CI 1.12–1.76 for the high-exposure group of over 1.0 mg-day/m3). The study controlled for sex, age, race or ethnicity, rank, smoking history, and self-reported exposure. When exposure was classified as number of days with exposure at 65 µg/m3 or greater, the risk of asthma also increased with longer exposures. Study strengths include the objective exposure assessment and the use of physician-diagnosed asthma as the basis of clinical evaluations. Limitations include the lack of pulmonary function data and specified criteria for the diagnosis of asthma, and self-selection into the DoD registry.
A study of a 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 2002). Five years after the war, veterans were asked about their exposures and current symptoms. 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 authors ascribed the different results for self-reported and objective exposure measurement to recall bias. Population-based sampling, which implies that findings can be generalized to all military personnel in the Persian Gulf, is a strength; however, it is limited by poor case definitions and disease misclassification.
In a postwar hospitalization study of 405,142 active-duty Gulf War veterans, Smith et al. (2002) also examined the effect of oil-well-fire exposure. There was no association between exposure to the fires and the risk of hospitalization for asthma (relative risk [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 a modest nonsignificant increase in the relative risk of emphysema (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.
Respiratory Disease in OEF/OIF Veterans Exposed to Burn Pits
The DoD report (AFHSC et al. 2010) describing several epidemiologic investigations of health outcomes among military personnel deployed to Iraq and Afghanistan included results on respiratory diseases. The investigators compared incidence rates of diseases and disorders at two military bases in Iraq with burn pits (JBB and Camp Taji) and with four comparison groups (nondeployed personnel in the United States, those deployed to two sites without burn pits in Kuwait [Camps Arifjan and Buehring], and those deployed to Korea). Those potentially exposed to burn pits at JBB or Camp Taji in Iraq consistently showed significantly lower or similar adjusted incidence rate ratios when compared with the nondeployed group. Incidence rate ratios (IRRs) were
2The following text was excerpted from IOM (2006).
decreased among personnel deployed to JBB and Taji for respiratory diseases and acute respiratory infections, while estimates were significantly lower in JBB (not significant in Taji) for COPD, asthma, and sleep apnea with all risk estimates for both bases being less than one. However, personnel without exposure to burn pits at Camps Arifjan and Buehring in Kuwait, and at the Korean base had similarly reduced or nonsignificant IRRs, indicating a healthy warrior effect but no disease potentially associated with being deployed to sites with burn pits.
The DoD report also included details of a Millennium Cohort Study analysis that found no significant differences in newly diagnosed asthma, bronchitis, emphysema, or self-reported respiratory symptoms between those deployed to areas within 5 miles of burn pits and those not exposed. No increased risk was noted with increasing cumulative exposure (days) or by camp site. Analyses were adjusted for smoking status, physical activity, and other covariates measured at baseline (AFHSC et al. 2010).
Cases of bronchiolitis have been reported in the media, presumably from exposure to the Mosul sulfur fire in Iraq in 2003 (Bartoo 2010). Constrictive bronchiolitis (CB), also known as bronchiolitis obliterans, is a narrowing of the small airways (the bronchioles) in the lungs. It can be irreversible and can impair daily functioning to the extent that affected individuals are no longer fit for military duty. There are multiple causes, including rheumatoid arthritis, inhalation of toxicants, rejection of a transplanted lung, or it might be idiopathic. It can only be diagnosed by lung biopsy, an invasive procedure that requires a hospital stay, and there is no accepted treatment (King et al. 2008; Bartoo 2010).
Preliminary reports described an unexpected number of CB cases among military personnel who had lung biopsies to determine the cause of their shortness of breath (King et al. 2008; Miller 2009; Bartoo 2010). A total of 38 soldiers were diagnosed with constrictive brochiolitis among 49 who underwent lung biopsy (out of 80 soldiers who had served in Iraq and/or Afghanistan and were referred for respiratory problems). Of the cases, 87% reported exposure while deployed to dust storms, 74% to the 2003 sulfur fire in Mosul, Iraq, and 63% to incinerated waste. Compared to a group of healthy soldiers, the cases were significantly (p < 0.001) older; had a higher BMI; had reduced pulmonary function measures for FEV1, FVC, and capacity to diffuse carbon monoxide; and had worse results for several cardiopulmonary tests (King et al. 2011).
In response to these cases of CB, the US Army Surgeon General requested a further study by CHPPM at Fort Campbell, Kentucky (USAPHC 2010). The exploratory analysis of chronic or recurring lung disease among veterans exposed to the Mosul sulfur fire in 2003 (191 Army firefighters and 6,341 soldiers located within 50 km of the fire) compared with unexposed deployed troops found no association between exposure to the fire and CB, but the possibility of health effects could not be ruled out. Follow-up was conducted through June 2007. Comparison of morbidity among firefighters and the exposed brigade to two control populations provided mixed results. Compared to unexposed controls in the Q-west area, standardized mortality ratios (SMRs) were significantly decreased for respiratory diseases (acute respiratory infections, COPD, asthma, circulatory diseases, ill-defined conditions, signs and symptoms involving the cardiovascular system, and signs and symptoms involving the respiratory system, all SMRs less than 0.74 and p < 0.05, for the exposed firefighters and the exposed brigade. Compared to the general unexposed population, the exposed brigade was diagnosed with more respiratory diseases (SMR 1.13, 95% CI 1.08–1.18), acute respiratory infections (SMR 1.18, 95% CI 1.12–1.24), and signs, symptoms, and ill-defined conditions involving respiratory system and chest (SMR 1.08, 95% CI 1.0–1.17), whereas SMRs for other disease groups were not significant and significant differences were not reported between the firefighters and the general unexposed population. The authors note that demographic differences between exposed and unexposed groups might have introduced bias, especially as those exposed tended to be younger. Despite the study’s limitations and potential biases, the authors reported no clear associations from this investigation but recommend follow-up and further study (USAPHC 2010).
Overall, the key and supporting studies showed no evidence of increased mortality from respiratory causes among firefighters. One small supporting study reported an increase in sarcoidosis prevalence (Prezant et al. 1999). There are no key studies of respiratory disease among incinerator workers or surrounding communities.
The two key studies of pulmonary function in firefighters show decreases in lung function using longitudinal
analyses while controlling for important factors such as smoking (Peters et al. 1974; Sparrow et al. 1982). Supporting studies of pulmonary function among firefighters show a wide range of results, however, with only a few of them showing decreased pulmonary function in firefighters (Unger et al. 1980; Tepper et al. 1991; Liu et al. 1992; Serra et al. 1996; Betchley et al. 1997; Mustajbegovic et al. 2001). Two of three supporting studies of incinerator workers show decreased pulmonary function after a few years of follow-up; these studies adjusted for other causes of decreased function and symptoms and decreases specific to job-related exposures (Hours et al. 2003; Charbotel et al. 2005). No key, but several supporting studies describe community exposure to incinerator emissions as part of the Health and Clean Air Study; however, those studies do not indicate any increased risks of respiratory effects.
In conclusion, the committee finds that there is inadequate/insufficient evidence to determine whether an association exists between respiratory disease and combustion products in the populations discussed here. However, several studies that found reductions in pulmonary function among firefighters and incinerator workers provide limited/suggestive evidence for an association between exposure to combustion products and decreased pulmonary function in these populations.
DISEASES OF THE NERVOUS SYSTEM
Diseases of the nervous system encompass genetic, degenerative, and traumatic damage to the brain, spinal cord, and nerves. Risk factors for specific neurologic disorders include age, family history, infections, traumatic injuries, and exposure to environmental toxicants. Neurologic outcomes range from changes in cognitive function, headache, nerve or bodily pain, to epilepsy, amyotrophic lateral sclerosis (ALS), Parkinson’s disease, and multiple sclerosis (MS). The committee identified only a few studies of neurologic diseases that were attributed to exposures similar to those expected from the burn pits. No studies of neurologic effects in communities surrounding incinerators were identified.
Neurologic Disease in Firefighters
The committee identified only one key study of neurologic outcomes in firefighters. Baris et al. (2001) conducted a retrospective cohort mortality study of neurologic effects in 7,789 structural firefighters in Philadelphia employed between 1925 and 1986 and a reference group of the general U.S. white male population. The firefighters worked for an average of 18 years, with a 26-year average follow-up. The measures of exposure included duration of employment, type of company employment, year of hire, cumulative number of fire runs, and fire runs during first 5 years as a fireman, as well as lifetime fire runs with diesel exposure. Based upon 12 firefighter deaths, no increase in deaths from nervous system diseases was observed (SMR 0.47, 95% CI 0.27–0.83).
Two studies have reported central nervous system effects (Kilburn et al. 1989; Bandaranayke et al. 1993) in firefighters exposed to polychlorinated biphenyls (PCBs) and other chemicals from specific events. Bandaranayke et al. (1993) found that 245 firefighters exposed to a chemical fire were more likely to experience nervous system effects as evidenced by poor neuropsychological test responses, but effects from chronic anxiety could not be ruled out. Kilburn et al. (1989) reported impaired memory and cognitive function among 14 firefighters exposed to PCBs, but the study quality is poor, and a reanalysis of the data suggested that most of the significant findings could be due to chance alone (Mustacchi 1991). Additionally, several cohort studies (Vena and Fiedler 1987; Beaumont et al. 1991; Grimes et al. 1991; Guidotti 1993; Tornling et al. 1994; Ma et al. 2005) also failed to find an increased risk for neurologic disease among firefighters exposed to chemical or other types of fires.
Neurological Disease in Incinerator Workers
No key studies of neurologic effects among those occupationally exposed to emissions from incinerators were identified by the committee.
Gustavsson (1989) found no increase in mortality from nervous system diseases among a cohort of 176 incinerator workers in Stockholm, Sweden, when compared to national and local mortality rates (SMR 1.33, 95% CI 0.03–7.39; SMR 1.32, 95% CI 0.03–7.36, respectively).
Neurologic Disease in Gulf War Veterans Exposed to Oil-Well–Fire Smoke
Several Gulf War studies evaluated the relationship between exposure to combustion products and neurobehavioral effects (Iowa Persian Gulf Study Group 1997; Proctor 1998; Unwin et al. 1999; Kang et al. 2000; Spencer et al. 2001; White et al. 2001; Wolfe et al. 2002). These studies found a positive relationship between self-reported exposure and self-reported neuropsychological, cognitive, or mood symptoms. Because combustion product exposure was self-reported, the Gulf War and Health committee considered the studies to provide only weak evidence of an effect.
Smith et al. (2002) investigated hospitalization for mental disorders and nervous system diseases by categories of exposure to smoke from oil-well fires among Gulf War veterans; relative risk ranged from 0.79 to 0.96 (all nonsignificant). Barth et al. (2009), studying mortality from ALS, MS, and Parkinson’s disease, found no increased risk for any of these diseases among veterans potentially exposed to oil-well–fire smoke.
Neurologic Disease in OEF/OIF Veterans Exposed to Burn Pits
No studies of neurologic disease among OEF/OIF veterans were identified by the committee.
Occupational studies of firefighters and incinerator workers do not show increased rates of mortality or elevated prevalence of neurologic disease. Personnel serving in Iraq during the 1990–1991 Gulf War as firefighters and reporting exposure to oil-well–fire smoke had a greater prevalence of self-reported neurobehavioral effects than era veterans not reporting exposure; however, the increase could not be definitively associated with exposure to combustion products.
Based upon its review of the literature, the committee concludes that there was inadequate/insufficient evidence for an association between combustion products and nervous system disease or neurobehavioral effects in the populations studied.
DISEASES OF THE CIRCULATORY SYSTEM
Circulatory system diseases, often referred to as cardiovascular diseases (CVD), include many health outcomes pertaining to the heart and vascular tissues. Circulatory diseases include rheumatic heart disease; hypertension; ischemic heart disease; congestive heart failure; pulmonary heart disease and other forms of heart disease; cerebrovascular disease; diseases of the arteries, arterioles, capillaries, veins, and lymphatic vessels; and other circulatory system disorders.
The most common cause of circulatory disease is atherosclerosis, which is the formation of vascular lesions resulting from excessive lipid deposition and macrophage infiltration. Atherosclerosis is the main cause of cardio-
TABLE 6-1 Risk Estimates for Diseases of the Circulatory System in Firefighters and Incinerator Workers
|Study||Study Type||Population||Risk Estimate (95% CI)|
|Diseases of the Circulatory System|
|Aronson et al. 1994||K||Firefighters||SMR 0.99 (0.89–1.10)|
|Baris et al. 2001||K||Firefighters||SMR 1.01 (0.96–1.07)|
|Eliopulos et al. 1984||K||Firefighters||SMR 0.78 (0.60–1.01)|
|Guidotti et al. 1993||K||Firefighters||SMR 1.03 (0.88–1.21)|
|Heyer et al. 1990||K||Firefighters||SMR 0.78 (0.68–0.92)|
|Tornling et al. 1994||K||Firefighters||SMR 0.84 (0.71–0.98)|
|Vena and Fiedler 1987||K||Firefighters||SMR 0.92 (0.81–1.04)|
|Gustavsson 1989||K||Incinerator workers||SMR 1.06 (0.78–1.42)|
|Bates et al. 1987||S||Firefighters||SMR 1.73 (1.12–2.66)|
|Feuer and Rosenman 1986||S||Firefighters||PMR 1.02 (p > 0.05)|
|Grimes et al. 1991||S||Firefighters||SMR 1.16 (1.10–1.32)|
|Ma et al. 2005||S||Firefighters||SMR 0.69 (0.63–0.76)|
|Milham and Ossiander 2001||S||Firefighters||PMR 0.99 (p = 0.70)|
|Ma et al. 2005||S||Firefighters||SMR 0.73 (0.65–0.83)|
|Diseases of the Heart|
|Demers et al. 1992a||K||Firefighters||SMR 0.79 (0.72–0.87)|
|Guidotti et al. 1993||K||Firefighters||SMR 1.10 (0.92–1.31)|
|Beaumont et al. 1991||K||Firefighters||SMR 0.89 (0.81–0.97)|
|Chronic Rheumatic Heart Disease|
|Aronson et al. 1994||K||Firefighters||SMR 0.15 (0.004–0.85)|
|Milham and Ossiander 2001||S||Firefighters||PMR 0.73 (p = 0.28)|
|Milham and Ossiander 2001||S||Firefighters||PMR 0.82 (p = 0.20)|
|Ischemic Heart Disease|
|Aronson et al. 1994||K||Firefighters||SMR 1.04 (0.92–1.17)|
|Baris et al. 2001||K||Firefighters||SMR 1.09 (1.02–1.16)|
|Beaumont et al. 1991||K||Firefighters||SMR 0.95 (0.87–1.04)|
|Demers et al. 1992a||K||Firefighters||SMR 0.82 (0.74–0.90)|
|Eliopulos et al. 1984||K||Firefighters||SMR 0.84 (0.60–1.14)|
|Guidotti et al. 1993||K||Firefighters||SMR 1.06 (0.87–1.28)|
|Hansen 1990||K||Firefighters||SMR 1.15 (0.74–1.78)|
|Tornling et al. 1994||K||Firefighters||SMR 0.98 (0.81–1.17)|
|Dibbs et al. 1982||K||Firefighters||RR 0.5 (0.2–1.4)|
|Gustavsson 1989||K||Incinerator workers||SMR 1.26 (0.87–1.76)|
|Burnett et al. 1994||S||Firefighters||PMR 1.01 (0.97–1.05)|
|Calvert et al. 1999||S||Firefighters||PMR 1.04 (0.94–1.14) white|
|Calvert et al. 1999||S||Firefighters||PMR 1.69 (1.10–2.47) black|
|Deschamps et al. 1995||S||Firefighters||SM 0.74 (0.20–1.90)|
|Sardinas et al. 1986||S||Firefighters||SMR 1.52 (1.23–1.81)|
|Sardinas et al. 1986||S||Firefighters||MOR 1.07 (0.91–1.23)|
|Smith et al. 2002||Gulf War||RR 0.82 (0.68–0.99)|
|Aronson et al. 1994||K||Firefighters||SMR 1.07 (0.93–1.23)|
|Dibbs et al. 1982||K||Firefighters||RR 0.5 (0.1–1.9)|
|Pulmonary Embolism and Infarction|
|Milham and Ossiander 2001||S||Firefighters||PMR 0.80 (p = 0.55)|
|Aronson et al. 1994||K||Firefighters||SMR 0.76 (0.55–1.03)|
|Baris et al. 2001||K||Firefighters||SMR 0.83 (0.69–0.99)|
|Beaumont et al. 1991||K||Firefighters||SMR 0.84 (0.67–1.03)|
|Study||Study Type||Population||Risk Estimate (95% CI)|
|Demers et al. 1992a||K||Firefighters||SMR 0.85 (0.67–1.06)|
|Guidotti et al. 1993||K||Firefighters||SMR 0.39 (0.18–0.73)|
|Tornling et al. 1994||K||Firefighters||SMR 0.71 (0.44–1.09)|
|Vena and Fiedler 1987||K||Firefighters||SMR 0.92 (0.64–1.27)|
|Gustavsson 1989||K||Incinerator workers||SMR 0.45 (0.09–1.33)|
|Deschamps et al. 1995||S||Firefighters||SMR 1.16 (0.24–3.38)|
|Feuer and Rosenman 1986||S||Firefighters||PMR 0.63 (p > 0.05)|
|Grimes et al. 1991||S||Firefighters||SMR 1.13 (0.66–1.95)|
|Ma et al. 2005||S||Firefighters||SMR 0.80 (0.60–1.05)|
|Arteriosclerotic Heart Disease|
|Aronson et al. 1994||K||Firefighters||SMR 1.41 (0.91–2.10)|
|Guidotti et al. 1993||K||Firefighters||SMR 1.50 (0.77–2.62)|
|Heyer et al. 1990||K||Firefighters||SMR 0.75 (0.63–0.89)|
|Vena and Fiedler 1987||K||Firefighters||SMR 0.92 (0.79–1.07)|
|Feuer and Rosenman 1986||S||Firefighters||PMR 1.11 (p > 0.05)|
|Grimes et al. 1991||S||Firefighters||SMR 1.09 (0.89–1.35)|
|Milham and Ossiander 2001||S||Firefighters||PMR 1.02 (p = 0.39)|
|Diseases of Arteries|
|Milham and Ossiander 2001||S||Firefighters||PMR 0.94 (p = 0.56)|
|Aronson et al. 1994||K||Firefighters||SMR 2.26 (1.36–3.54)|
|Diseases of Veins|
|Aronson et al. 1994||K||Firefighters||SMR 1.68 (0.72–3.31)|
|Milham and Ossiander 2001||S||Firefighters||PMR 1.10 (p = 0.70)|
|Other Circulatory Diseases|
|Beaumont et al. 1991||K||Firefighters||SMR 0.88 (0.73–1.04)|
|Demers et al. 1992a||K||Firefighters||SMR 0.96 (0.80–1.14)|
|Eliopulos et al. 1984||K||Firefighters||SMR 0.65 (0.38–1.07)|
|Deschamps et al. 1995||S||Firefighters||SMR 0.84 (0.02–4.68)|
|Other Heart Diseases|
|Milham and Ossiander 2001||S||Firefighters||PMR 0.98 (p = 0.81)|
|Hu et al. 2003||S||Incinerator workers||OR 2.8 (1.0–7.9)|
NOTE: Risk estimates in bold italics denote significant differences in risk. K = key study; S = supporting study.
vascular mortality associated with acute myocardial ischemia, heart failure, and stroke. Patients with myocardial ischemic injury often have arrhythmias, hypertrophy, cardiomyopathy, and heart failure. Several risk factors are known to contribute to overall circulatory disease including elevated low-density lipoprotein (LDL cholesterol), increased blood pressure, diabetes mellitus, tobacco use, poor diet, obesity, excessive alcohol use, and physical inactivity (CDC 2009).
Studies on circulatory outcomes in firefighters, incinerator workers, communities near incinerators, and Gulf War veterans are discussed below. Because of the large number of studies with risk estimates for multiple circulatory outcomes, the results have been summarized in Table 6-1 by specific circulatory effect. This section uses disease terminology as cited by study authors.
Circulatory Disease in Firefighters
The committee reviewed several studies reporting circulatory disease mortality and one measuring disease incidence in firefighters to assess whether occupational exposure to combustion products affects circulatory disease. A majority of those studies were designed to evaluate all-cause mortality with circulatory disease as a sub-category of evaluation.
Aronson et al. (1994) conducted a retrospective cohort mortality study of 5,414 firefighters in metropolitan Toronto with 777 deaths. SMRs for diseases of veins, cerebral vascular disease, and chronic rheumatic heart disease were not elevated compared to the general male population of Ontario after adjusting for age and calendar period. Ischemic heart disease accounted for 289 deaths (SMR 1.04, 95% CI 0.92–1.17), of which 205 were due to acute myocardial ischemia (SMR 1.07, 95% CI 0.93–1.23). A statistically significant excess of myocardial infarction was apparent at 20–24 years since first employment (SMR 1.56, 95% CI 1.03–2.25), but no trend was apparent. Arteriosclerosis accounted for 24 deaths (SMR 1.41, 95% CI 0.91–2.10), 19 of which were attributed to aortic aneurysm (SMR 2.26, 95% CI 1.36–3.54). No deaths from aortic aneurysm occurred prior to 20 years since first employment. However, at 20–30 years since first employment the SMR was 3.03 (95% CI 0.63–8.86); at 40–49 years since first employment the authors observed a statistically significant SMR of 2.95 (95% CI 1.27–5.82). The majority of deaths (17 of 19) occurred in firefighters who worked 25 years or more (SMR 2.50, 95% CI 1.46–4.00). The authors concluded that while this study provides some evidence of an association between occupation as a firefighter and risk of aortic aneurysms, the result might be due to chance because knowledge at the time did not support an occupational etiology.
Baris et al. (2001) conducted a retrospective cohort mortality study to assess cancer mortality among 7,789 firefighters in Philadelphia compared to the mortality of U.S. white men. The authors found a significant excess risk for ischemic heart disease (SMR 1.09, 95% CI 1.02–1.16). No significant association was found for circulatory diseases, and a decreased risk of cerebrovascular disease was noted (SMR 0.83, 95% CI 0.69–0.99). There were no positive exposure-response trends for any outcome across increasing years of employment or number of runs. Results were not consistent across strata when grouped by company type (engine, ladder, or both) or by date of hire. Outcomes associated with diesel exposure could not be assessed due to the small number of diesel-exposed firefighters and short follow-up.
A mortality study of San Francisco firefighters by Beaumont et al. (1991) found fewer cardiovascular deaths than expected among 3,066 firefighters employed from 1940 to 1970 and followed through 1982. There were 508 deaths from diseases of the heart and 131 other circulatory deaths. Incidence density rate ratios, indirectly standardized for age, sex, year, and race based on person-years at risk, compared the firefighters to the general U.S. population. A significant decrease in heart diseases was seen (RR 0.89, 95% CI 0.81–0.97). The risk of ischemic heart disease, other circulatory diseases, and cerebrovascular disease was decreased for firefighters, but not significantly.
The mortality of 4,546 male firefighters from three northwestern U.S. cities was assessed by Demers et al. (1992a) compared to police officers. No significantly elevated risks were noted. Rather, significantly reduced risks were found for heart disease (SMR 0.79, 95% CI 0.72–0.87; incidence density ratio [IDR] 0.86, 95% CI 0.74–1.0) and ischemic heart disease (SMR 0.82, 95% CI 0.74–0.90; IDR not significant). SMRs were reduced but not significantly for other circulatory diseases and cerebrovascular disease; however, the IDRs were 0.72 (95% CI 0.54–0.96) and 0.65 (95% CI 0.45–0.92), respectively. Neither SMR nor IDR were significant for diseases of arteries, veins, and pulmonary circulation. Incorporating a 10-year lag showed an SMR of 2.55 (95% CI 1.43–3.38) for diseases of arteries, veins, and pulmonary circulation among those with 30 or more years of exposure. Furthermore, when SMRs were stratified by duration of employment, years since first employment, and age, those in the highest categories had significantly elevated SMRs for diseases of arteries, veins, and pulmonary circulation. A previous analysis of this cohort was published by Rosenstock et al. (1990) who reported an SMR of 0.81 (95% CI 0.73–0.89) for nonmalignant circulatory diseases compared to the white U.S. male population.
Dibbs et al. (1982) conducted a cohort study of firefighters enrolled in the Normative Aging Study, a longitudinal study of aging among veterans. Four of the 171 firefighters (2.3%) developed coronary heart disease
compared with 71 (4.8%) of 1,475 non-firefighters. The estimated RR for myocardial infarction was 0.5 (95% CI 0.1–1.9) and 0.5 (95% CI 0.2–1.4) for coronary heart disease, indicating a lower rate of disease among firefighters compared with non-firefighters. Risk factors including serum cholesterol, systolic and diastolic blood pressures, body mass index, and cigarette smoking were assessed. Only the percentage of smokers varied between firefighters and non-firefighters (41.5% vs. 35.7%). Relative risks were not adjusted for any covariates other than age.
Glueck et al. (1996) prospectively followed a cohort of 806 firefighters in Cincinnati, Ohio, who underwent a series of physical exams, blood tests, and cardiac tests. In the 8-year follow-up period there were 7 myocardial infarcts and 15 coronary heart disease (CHD) cases without infarction. The firefighters were significantly heavier, older, had higher systolic blood pressure, and longer follow-up than the comparison group of healthy, employed men taking part in the National Health and Nutrition Examination Survey I (NHANES I) without CHD. There were slightly fewer myocardial infarcts among the firefighters compared with the control group (1.35/1,000 person-years vs. 2.07/1,000 person-years, p = 0.1). It should be noted that at study entry, firefighters who sustained CHD were significantly older; had higher diastolic and systolic blood pressures; smoked more per day; had higher LDL, triglycerides, and total cholesterol; were more likely to have a family member with CHD; and had a shorter follow-up time (p < 0.05) than firefighters who did not develop CHD. Those who developed CHD also had a longer length of employment (22.2 years vs. 18 years, p = 0.052). Twenty-six firefighters reported having experienced smoke inhalation but did not develop CHD. No increase in the risk of CHD among firefighters was observed. The authors concluded that CHD risk among firefighters is due primarily to conventional and modifiable risk factors (blood pressure, cholesterol, and smoking).
Studying a subpopulation of that reported by Demers et al. (1992a), Heyer et al. (1990) studied 2,289 male firefighters in Seattle who were employed between 1945 and 1980. Compared to the U.S. white males, SMRs for circulatory system disease mortality and specifically arteriosclerotic disease were significantly decreased in firefighters (SMR 0.78, 95% CI 0.68–0.92; SMR 0.75, 95% CI 0.63–0.89, respectively). When stratified by age, time since first employment and duration of exposure, those older than 65 years, those with less than 30 years since first exposure, and firefighters with less than 30 years of exposure, were all significantly less likely to die from circulatory diseases. A subgroup of individuals surviving 30 years or more after their first exposure revealed a trend (p < 0.10) of increasing risk with increasing exposure for circulatory system disease; firefighters with 30 years or more of fire combat duty had a RR of 1.84 compared with those with less than 15 years of fire combat duty.
Eliopulos et al. (1984) conducted a retrospective cohort mortality study of 990 male firefighters employed by the Western Australian Fire Brigade between 1939 and 1978. With 16,876 person-years of follow-up and 116 deaths, the authors found no evidence of increased mortality from CVD when compared to deaths of West Australian males, adjusted for age and calendar time. The nonsignificant SMRs for circulatory disease (55 deaths), ischemic heart disease (39 deaths), and other circulatory diseases (16 deaths) were 0.78, 0.84, and 0.65, respectively.
Guidotti et al. (1993) conducted a retrospective cohort mortality study of 3,328 firefighters employed between 1927 and 1987 in Edmonton and Calgary, Alberta. Vital status for 96% of the cohort was ascertained, resulting in 370 deaths and 64,983 person-years. An exposure opportunity index term, reflecting estimates of the relative time spent in close proximity to fires by job classification, was applied to refine exposure data based on years of service. The authors found that mortality from heart disease was close to that expected (SMR 1.10; 95% CI 0.92–1.31) compared to the male population of Alberta when adjusted for age and calendar period. Specific causes (ischemic heart disease and arteriosclerosis) were also not significantly elevated among the firefighters and the risk of cerebrovascular disease was lower (SMR 0.39, 95% CI 0.18–0.73). No significant trends or associations were noted when stratified by exposure index or latency. The authors could not assess potential confounders and expressed concern about a lack of power when assessing trends and multiple strata.
A study of mortality among firefighters in Denmark was reported by Hansen (1990). The cohort of 866 male firefighters was identified from the 1970 nationwide census of public employees aged 15 to 69 years old. Male civil servants and public employees in the same age range (n = 47,694) employed in physically demanding jobs were used as a comparison group adjusted for age and calendar period. There were 57 deaths among firefighters and 2,383 deaths in the comparison group at 10 years of follow-up. The SMR was 1.15 (95% CI 0.74–1.71) for ischemic heart disease; however, when stratified to compare the first and last 5 years of follow-up, the SMR for the former was 1.48 (95% CI 0.74–2.65) and 0.97 (95% CI 0.52–1.66) for the latter. Other cardiovascular causes of
death were not reported. While the comparison group was selected to resemble the firefighters based on physical fitness and strength, social class, geographic distribution, and stability of employment to minimize the effects of a healthy worker bias, the groups might differ in lifestyle.
In Stockholm, Tornling et al. (1994) examined the mortality of 1,116 male firefighters employed for at least a year between 1931 and 1983 and followed through 1986. Exposure was determined from 10% of all reports of all fires in Stockholm (19,000 reports examined). An exposure index was created based on number of fires fought each calendar year and use of self-contained breathing apparatus. SMRs were standardized for age, calendar year, and sex using the Stockholm population. For circulatory diseases, the SMR was 0.84 (95% CI 0.71–0.98); ischemic heart disease was 0.98 (95% CI 0.81–1.17), and cerebrovascular disease was 0.71 (95% CI 0.44–1.09). While generally not significantly elevated, SMRs for ischemic heart disease showed a tendency to increase with older age and latency. When stratified by duration of employment and number of fires, however, no trends were evident and no significant associations were noted.
Vena and Fiedler (1987) compared mortality of 1,867 white male firefighters in Buffalo, New York, with mortality of U.S. males with adjustment for age. The SMRs were 0.92 (95% CI 0.81–1.04) for all diseases of circulatory system, 0.92 (95% CI 0.79–1.07) for arteriosclerotic heart disease, and 0.92 (95% CI 0.64–1.27) for all central nervous system (CNS) vascular lesions. No increase in circulatory deaths was observed when stratified by duration of employment, calendar year of death, year of hire, or latency.
Using a subpopulation of the cohort studied by Aronson et al. (1994), Bates (1987) compared 646 firefighters employed by the Toronto Fire Department with all men living in the city of Toronto. The authors identified 21 firefighter deaths due to coronary artery disease (out of 52 total deaths) and reported no significant association between death from circulatory disease and firefighting activity or year of death. Studying ischemic heart disease in firefighters in Connecticut, Sardinas et al. (1986) reported a slightly elevated SMR of 1.52 (95% CI 1.23–1.81) and mortality odds ratio (MOR) of 1.07 (95% CI 0.91–1.23) compared to the general Connecticut population, but a significantly lower mortality among firemen when compared to policemen (MOR 0.62, 95% CI 0.56–0.68). In Washington State, (Milham and Ossiander 2001) found that age-adjusted proportional mortality ratios (PMRs) for circulatory disease, or any subcategories of circulatory disease (arteriosclerotic heart disease including coronary disease, other diseases of the heart, hypertensive disease, diseases of the arteries, diseases of the veins, or pulmonary embolism and infarction) were not elevated for firefighters and fire protection workers. Among 205 City of Honolulu firefighters, Grimes et al. (1991) found that cardiovascular mortality was slightly elevated, with a crude RR of 1.16 (95% CI 1.10–1.32). Slightly elevated but nonsignificant risks were reported for arteriosclerotic heart disease and all CNS vascular lesions; however, when stratified by ethnicity (Caucasian and Hawaiian), no associations were apparent.
Mortality of U.S. firefighters in 27 states was assessed by Burnett et al. (1994) using the National Occupational Mortality Surveillance system. There was no increase in ischemic heart disease deaths among firefighters. Another analyses of National Occupational Mortality Surveillance data investigated racial differences. Calvert et al. (1999) found that firefighters were among the 10 occupations with the highest PMRs for ischemic heart disease for black males (PMR 1.69, 95% CI 1.10–2.47) but not for white males.
In New Jersey, Feuer and Rosenman (1986) studied police and firefighters employed for at least 10 years in New Jersey and found increased risks of arteriosclerotic heart disease (PMR 1.22) compared to U.S. mortality; however, when compared with the New Jersey population, the PMR was slightly, but not significantly, elevated (PMR 1.11), and no excess was evident when compared to police officers. For circulatory deaths, no association was apparent compared to U.S. or New Jersey populations or to police officers. The investigators’ decision to use three different reference groups, particularly police who are likely to be more similar to firefighters than the general New Jersey or U.S. population, mitigates bias introduced by a healthy worker effect.
Exhibiting a strong healthy worker effect, Deschamps et al. (1995) found no association between ischemic heart disease (four deaths), other circulatory diseases (one death), or cerebrovascular disease (three deaths) and occupational firefighting for 830 Parisian firefighters compared with the general French male population after 14
years of follow-up. The authors noted a number of study limitations, particularly the small number of events (32 deaths overall). The study by Ma et al. (2005) also had a healthy worker effect but had a large population of 34,796 male and 2,017 female professional firefighters in Florida. When compared to general population of Florida and adjusted for age and gender, the authors found the risks of circulatory disease were significantly reduced for male firefighters but elevated for female firefighters (deaths attributed to circulatory system causes, for men SMR 0.69, 95% CI 0.63–0.76 and for women SMR 2.49, 95% CI 1.32–4.25; atherosclerotic heart disease for male firefighters SMR 0.73, 95% CI 0.65–0.83, and for female firefighters SMR 3.85, 95% CI 1.66–7.58).
Three reviews of CVD in firefighters were identified by the committee. Haas et al. (2003) assessed six studies of coronary artery disease mortality in firefighters, all discussed above, and found no convincing evidence of an association between firefighting and coronary artery disease. According to the authors, the bias imposed by any healthy worker effect was not as strong as expected for these studies. A review of 22 studies by Guidotti (1995), 14 of which are described in this chapter, showed no presumptive risk of CVD, COPD, or aortic aneurysm among firefighters. Taking a different approach to consider the healthy worker effect, Choi (2000) evaluated 23 studies of CVD in firefighters, 17 of which are described above. Before the reassessment to factor in the healthy worker effects, 7 of the 23 studies (Eliopulos et al. 1984; Hansen 1990; Grimes et al. 1991; Guidotti 1993; Aronson et al. 1994; Burnett et al. 1994; Deschamps et al. 1995) showed an increased risk and 16 showed no increase. After the reassessment, 11studies showed an increase in risk and 12 did not. Choi concluded that after considering the healthy worker effect, there is an increased risk of death from heart disease among firefighters, but there is insufficient evidence of an increased risk of death from aortic aneurysm or of an association between firefighting and any heart disease subtype, such as MI. However, Choi could not eliminate confounding factors as the cause of the apparent increase in risks.
Circulatory Disease and Incinerator Workers
Gustavsson (1989) assessed mortality among 176 municipal waste incinerator workers near Stockholm, Sweden. Using national and local mortality rates to calculate SMRs, the risks for circulatory diseases, ischemic heart disease, or cerebrovascular diseases was not increased among incinerator workers. When stratified by length of employment, incinerator workers, compared with the local population, had an elevated death rate due to ischemic heart disease (SMR 1.86, p < 0.01) after more than 40 years after first employment, but not for shorter employment. Ischemic heart disease mortality rates were also elevated among those with more than 30 years of employment (SMR 1.67, p < 0.05), but not for less than 30 years.
No supporting studies of circulatory disease among municipal incinerator workers were identified by the committee.
Circulatory Disease in Communities Near Incinerators
No studies of circulatory disease among people living near incinerators were identified by the committee.
Circulatory Disease in Gulf War Veterans Exposed to Oil-Well–Fire Smoke
Among the studies of disease in Gulf War veterans, one key study examined CVD associated with exposure to oil-well fires.3 Morbidity in the form of post-war hospitalizations at DoD medical facilities of 405,142 active-duty
3This paragraph is based on text from IOM (2010). The current committee did not review the study, rather it relied on the assessment of the prior IOM committee that examined the evidence and weighed the health effects literature on this type of exposure and cardiovascular outcomes.
military personnel deployed to the Gulf War during the time of the fires in Kuwait (February 2, 1991, to October 31, 1991) was examined by Smith et al. (2002). Hospitalizations between 1991 and 1999 for diseases of the circulatory system were evaluated. Exposure to oil-well–fire smoke was estimated by combining smoke-plume modeling data and troop unit location. Exposure was categorized into seven levels based on combinations of average daily exposure (none, 1–260 µg/m3, or > 260 µg/m3) and duration of exposure (1–25 days, 26–50 days, or > 50 days). Compared with military personnel with no exposure to smoke from oil-well fires, there was no increase in the incidence of hospitalization for cardiovascular disorders at any level of exposure; relative risks ranged between 0.9 and 1.2 for the different levels of exposure without a clear dose-response trend. Relative risks were significantly decreased among those exposed to 1–260 µg/m3 for 26–50 days and > 50 days, and those exposed to > 260 µg/m3 for > 50 days. Veterans exposed to oil-well fires had a slightly lower risk than unexposed veterans for hospitalizations for ischemic heart disease (RR 0.82, 95% CI 0.68–0.99). This study provided individual level quantifiable exposure estimates but did not include confounding behavioral and environmental exposures. A limitation of this study is that health effects needed to be severe enough for hospital admission and, thus, less severe outcomes might be missed.
Circulatory Disease in OEF/OIF Veterans Exposed to Burn Pits
The DoD determined incidence relative risks for health outcomes in military personnel deployed to sites with burn pits (JBB and Taji in Iraq), to sites without burn pits (Arifan, Buehring, and Korea), and non-deployed personnel with 3 years of follow-up. Personnel at JBB reported fewer cases of circulatory system diseases (IRR 0.94, 95% CI 0.90–0.98) and cardiovascular signs and symptoms (IRR 0.81, 95% CI 0.74–0.88) compared with nondeployed military personnel, whereas personnel stationed at Taji were no different than nondeployed personnel. However, personnel deployed to Korea and to Arifan and Buehring in Kuwait (all without any potential exposure to burn pits) had similarly reduced or not significant incidence relative risks. CVD potentially associated with being deployed to a site with burn pits was not observed (AFHSC et al. 2010).
Based on the 25 studies of firefighters, incinerator workers, communities around incinerators, and veterans from Gulf War and OEF/OIF, two key studies (Aronson et al. 1994; Baris et al. 2001) provide support for an increased risk of certain cardiovascular outcomes in firefighters. Most studies assessed multiple cardiovascular outcomes including all circulatory disease, heart disease, arteriosclerosis, aortic aneurysm, myocardial infarction, cerebrovascular disease, other circulatory diseases, and diseases of the arteries and veins. Increased risks for any specific cardiovascular outcome were not consistently observed in these studies. Results of these studies were affected by several limitations, particularly the inability to control for confounding and inadequate follow-up time. A healthy worker bias was introduced by the use of inappropriate control groups in many studies, such as the use of general U.S. or local populations; however, some studies attempted to use other occupational groups such as police officers to correct for this bias. Lastly, as is true for many studies in this chapter, the lack of exposure assessment makes it difficult to determine whether a possible increase in the risk of CVD can be attributed to exposure to combustion products.
Based on its review of the epidemiologic literature, the committee concludes that there is insufficient/inadequate evidence of an association between long-term occupational exposure to combustion products and circulatory disease in the populations studied.
ADVERSE REPRODUCTIVE AND PERINATAL OUTCOMES
Potential effects of parental exposure to combustion products on reproductive and perinatal health were of concern to the committee. Chemical exposures may affect fertility, maternal health, birth weight, infant health and development, twinning, or fetal and infant death. The committee reviewed studies on adverse reproductive and
perinatal outcomes in children born to parents with three different exposure scenarios: firefighters, people living in communities near municipal incinerators, and military personnel deployed in the 1990–1991 Gulf War or OEF/OIF.
Birth Defects in Children of Male Firefighters
The following studies assess birth defects among live-born children of male firefighters. No studies assessing other adverse reproductive outcomes such as fetal death, infant death, low birth weight, and infertility among firefighter populations were identified. Sample sizes are small, and while maternal demographic characteristics are considered, there is no adjustment for maternal exposures to smoke or other toxicants during pregnancy.
No key studies of birth defects in children of male firefighters were identified by the committee.
Olshan et al. (1990) evaluated data on 89 malformed children born to 271 British Columbia firefighters in 1952–1973, matched against 174 normal children born to 749 policemen and normal children born to 21,929 fathers in all other occupations by month, year, and hospital of birth. Focused on heart defects, these investigators found heart defects to be strongly associated with parental firefighting as an occupation: specifically, ventricular defects (OR 2.30, 95% CI 0.77–6.92 compared with all other occupations, and OR 5.05, 95% CI 1.43–17.82 compared with police), atrial defects (OR 6.81, 95% CI 1.40–33.16 compared with all other occupations, and OR 3.82, 95% CI 1.19–12.33 compared with police); and patent ductus arteriosis (OR 1.69, 95% CI 0.45–6.39 compared with all other occupations, and OR 14.6, 95% CI 1.03–206.16 compared with police). Odds ratios were elevated but not significant for several other categories including microcephalus, cleft lip, pyloric stenosis, and urinary tract obstructive defects, with some adjustments for low birth-weight and prematurity. The investigators suggest that children of firefighters are at increased risk of ventricular and atrial septal defects, with wide confidence intervals for the other elevated risk categories.
Two subsequent case-control studies do not corroborate the cardiac findings reported by Olshan et al. (1990), Aronson et al. (1996) compared 9,340 children with congenital heart defects, all born from 1979 to 1986, with 9,340 healthy controls randomly selected from the Ontario birth certificate file, and matched by birth year, maternal age, birth order of the child, birthplace of each parent (born in Ontario vs. not born in Ontario), and marital status of the mother at the time of birth. Eleven cases and 9 controls were born to fathers employed as firefighters (OR 1.22, 95% CI 0.46–3.33). The authors concluded that there was no association between firefighting as an occupation and the kinds of cardiac defects identified by Olshan et al. (1990). Like Aronson et al. (1996), Schnitzer et al. (1995) were not able to corroborate the findings reported by Olshan et al., and did not detect increased risk of ventricular or atrial defects among children of firefighters. Schnitzer et al. (1995) examined 28 categories of major birth defects in children born to Atlanta firefighter fathers, 1968–1980, compared to fathers with malformed children in all other occupations, matched for race, year, and hospital of birth. There were increased risks for cleft palate (OR 13.3, 95% CI 4.0–44.4), other heart defects (OR 4.7, 95% 1.2–17.8), hypospadias (OR 2.6, 95% CI 1.1–6.2), and club foot (OR 2.9, 95% CI 1.4–6.0).
Two other publications reviewed those studies on reproductive outcomes among the offspring of male firefighters. McDiarmid and Agnew (1995) concluded that measures should be taken to protect male and female firefighters from reproductive toxicity of harmful chemicals, especially for pregnant firefighters given the particular sensitivity of the human fetus to carbon monoxide. In their review of epidemiologic studies on paternal occupations and birth defects, Chia and Shi (2002) cite these studies but also emphasize the studies’ weaknesses and the need for more rigorous studies.
Reproductive Outcomes for Incinerator Workers
No key studies on reproductive outcomes and occupational exposures among incinerator workers were identified by the committee.
No supporting studies of reproductive outcomes among incinerator workers were identified by the committee.
Reproductive Outcomes for Parents Living Near Incinerators
No key studies pertaining to reproductive effects among people living near incinerators were reviewed by the committee.
The committee reviewed eight community-based incinerator studies in two general outcome categories: the first five studies (Jansson and Voog 1989; Cresswell et al. 2003; Cordier et al. 2004; Tango et al. 2004; Vinceti et al. 2008) examined birth defects, stillbirths, and infant death, while the last three (Lloyd et al. 1988; Williams et al. 1992; Rydhstroem 1998) looked at twinning and sex ratios.
Several studies modeled exposure to dioxin, which was generally assumed to be from the incinerators under study. In Sweden, Jansson and Voog (1989) investigated six cleft lip or cleft palate births at a single hospital during a 6-month period in 1987 to families living within a 50-km radius of an incinerator compared with local rates of birth defects for 18 Swedish boroughs. The authors concluded that modeled dioxin exposure did not explain the cluster. Taking a wider ecologic approach, no difference in local incidence rates of cleft lip or cleft palate births for each borough that installed incinerators from 1972 to 1986 was detected. The investigators suggested that no increased risk of cleft lip or cleft palate could be demonstrated in the study areas since the start of incineration practices but because of the small study group, observations could be attributed to chance. Tango et al. (2004) studied registry-based births in Japan to examine adverse reproductive effects associated with maternal residence within 10 km of one of 63 incinerators with high levels of dioxin emissions (> 80 ng-TEQ/m3). Reporting on a wide range of reproductive outcomes (low birth-weight, very low birth-weight, neonatal deaths, all congenital malformations combined, etc.), there was no significant excess of adverse reproductive effects to women living within 2 km of the incinerators including 225,215 live births from 1997–1998. However, the ratio of observed to expected neonatal deaths declined with increasing distance from the incinerators up to 10 km (p = 0.023 for infant deaths and p = 0.047 for infant deaths with all malformations combined). Drawing cases from hospital discharge records and a regional birth defects registry for 2003–2006, Vinceti et al. (2008) found no significantly increased risks or dose-response trends for birth defects or spontaneous abortion among women living (residential cohort) or working (occupational cohort) in the vicinity of the municipal incinerator in Modena, Italy, compared to women in the remaining municipal population. Areas of high and intermediate exposure were defined using meteorological data to estimate deposition of dioxins and furans in the study area. The analysis was limited by having few cases.
Cordier et al. (2004) studied congenital anomalies in 194 exposed communities in the vicinity of 70 different incinerators in the Rhone-Alps region of southeastern France. The overall rate of congenital anomalies was not higher in exposed communities compared with 2,678 neighboring unexposed communities (RR 1.04), after adjusting for year of birth, maternal age, department, population density, and average family income (modeled using distance to incinerator, dispersion modeling, and semi-quantitative dioxin emission estimates). A few congenital anomalies showed excess risks including facial clefts (RR 1.30, 95% CI 1.06–1.59) and renal dysplasia (RR 1.55,
95% CI 1.10–2.20). The report concludes that both incinerator emissions and road traffic density might explain some of the reported excess risk. In another birth defects registry study, Cresswell et al. (2003) compared congenital anomalies in two different geographic areas defined by distance from an incinerator in the British city of Newcastle-on-Tyne that started operation in 1988. Out of 81,255 live births between 1985–1999, there were 428 cases of birth defects in families residing within 3 km and 1,080 cases residing within 3–7 km of the incinerator. Investigators reported no significant association between the number of anomalies and residential proximity to the incinerator; however, rates of congenital abnormalities became significantly higher in 1998 and 1999 (RRs of 1.56 and 2.05, respectively) compared with the earlier years. Investigators were unable to explain the results for the last 2 years of the study without information on cumulative exposure or increases in exposure over later years.
Responding to anecdotal reports of increased twinning in cattle presumably due to pollutants from two incinerators in central Scotland, Lloyd et al. (1988) compared single/twin birth rates in hospitals in areas exposed to incinerator pollutants for the years 1975 to 1983. They concluded that the increased frequency of human twinning in areas most affected by incinerators, and supported by an anecdotal increase in twinning among dairy cattle, warrants further epidemiologic study. Studying the same population, Williams et al. (1992) reported a significant excess in female births (m:f ratio of 0.87, p < 0.05) at a location identified as most at risk from incinerator-based air pollution, but the ratio for the three risk areas combined was 1.01. The m:f ratio for the comparison areas combined was 0.99 and the ratio for Scotland was 1.06. In another study conducted in Sweden, Rydhstroem (1998) looked at twin deliveries before and after the commissioning of 14 incinerators between 1973 and 1990. Comparing recorded twin births against the expected number standardized for maternal age and year of delivery for all Swedish parishes, the authors report no apparent increase in the number of parishes or municipalities with a relative excess of twin deliveries, and no spatial clustering after the incinerators were commissioned.
Reproductive Outcomes for Gulf War Veterans Exposed to Oil-Well–Fire Smoke
An IOM study (2005) examined the scientific literature for associations between illness and exposure to toxic agents associated with Gulf War service. This review of more than 60 studies examined a broad range of reproductive and developmental outcomes, including fertility, preterm birth, low birth-weight, birth defects, and childhood cancers. Using the same classification system as in this report, that committee concluded that the evidence was inadequate/insufficient to determine whether an association exists between parental exposure to fuels such as kerosene, gasoline, and diesel, and adverse reproductive or developmental outcomes. That committee concluded there was limited/suggestive evidence of an association between parental exposure to combustion products such as PM10, NO2, SO2, and CO and pre-term birth and low birth-weight, but inadequate/insufficient evidence for other reproductive outcomes. The current committee did not review the studies in the 2005 report; but rather it relied on that committee’s published report and any new published studies.
As described in the IOM report on the health of Gulf War veterans (IOM 2010), Verret et al. (2008), in a study deemed to be supporting in that report, evaluated the effect of Gulf War deployment on the incidence of birth defects. When compared to 10-year prevalence data from the Paris Registry of Congenital Malformations, the prevalence of major anomalies did not differ between French Gulf War veterans and the general French population, with the exception of a decrease of Down syndrome among children born to veterans (prevalence rate ratio 0.36, 95% CI 0.13–0.78). The authors also conducted a nested case-control study. No associations were observed between birth defects and self-reported exposures to oil-well fire smoke, sandstorms, chemical alarms, or pesticides. To minimize recall bias, controls were restricted to veterans with at least one symptom-related hospitalization. However, the inclusion criterion was not applied equally to the cases; thus, control selection was plausibly related to exposure, and the results of the case-control analyses were subject to selection bias.
Reproductive Outcomes in OEF/OIF Veterans Exposed to Burn Pits
One preliminary epidemiologic investigation is described in a DoD report on a wide range of health outcomes among troops deployed to burn pit sites in Iraq and Afghanistan. This investigation, conducted by the NHRC (AFHSC et al. 2010), found no increase in the risk of preterm births or birth defects during the first year of life
in children born to women deployed before and during pregnancy (OR 1.19, 95% CI 0.89–1.64) out of 13,129 women deployed within a 5-mile radius of burn pits. No relationship with cumulative days of deployment or temporal proximity to conception were noted among mothers. For men deployed within a 5-mile radius of a burn pit anytime before the estimated date of conception (6,763 burn pit deployments out of 88,074 total deployed), there was no reported increase in premature births or birth defects (OR 0.98, 95% CI 0.86–1.12). However, the risk of unspecified birth defects increased if fathers were exposed more than 280 days prior to the estimated date of conception (OR 1.31, 95% CI 1.04–1.64), but no associations were noted with cumulative days of exposure.
The committee determined that there were no key studies of reproductive or perinatal outcomes among firefighters, incinerator workers, or communities near incinerators on which to base its conclusions. The supporting studies of birth defects in children of firefighters give mixed results, including uncorroborated reports of cardiac defects, cleft palate, hypospadias, and other defects. The studies raise questions, but they provided inadequate evidence of an association between working as a firefighter and birth defects of their children. While recognizing maternal exposure (and other maternal characteristics) as possible confounders, none of the studies appears to regard this information as critical to interpreting the results.
For children of populations living or working near incinerators, five supporting studies considered birth defects, stillbirths, and infant death. Three supporting studies examined twinning and/or sex ratios. Some elevated risks were reported, but investigators generally concluded there was no increased risk after adjustments. The committee noted several problems with these studies such as potential sources of misclassification of diagnosis, and exposure based on maternal work history, residential history, or birth registration errors. For most of the studies, maternal residence was determined at the time of birth, without data on the duration of residence in the study area relative to the pregnancy, introducing doubt about antenatal exposure in relation to windows of susceptibility for different fetal organ systems.
For children born to male and female personnel deployed in the Gulf and Iraq Wars, the committee found some evidence suggesting an association between adverse outcomes for preterm births and low birth-weight and parental exposure to combustion products, but not for birth defects or other outcomes, as detailed in the IOM reports (2005, 2010).
The committee concludes that there is insufficient/inadequate evidence to determine whether an association exists between parental exposure to combustion products and adverse effects in their children and other adverse reproductive and perinatal outcomes in the populations studied.
Exposure to environmental carcinogens is estimated to cause two-thirds of cancers (National Institute of Environmental Health Sciences 2003). While lifestyle, behavioral, and genetic factors are the most important known risk factors for cancer, many environmental exposures including mineralogical substances, infectious agents, biological toxins, radiation, pesticides, particulate matter and dust, solvents, exhaust, and a variety of industrial chemicals have been linked to cancer. Of importance to veterans potentially exposed to burn pit by-products, some types of particulate matter have been linked to lung and respiratory cancers; dioxins are highly carcinogenic; and PAHs have been linked to lung, skin, and urinary cancers (NIEHS 2003).
This section describes cancer incidence and mortality studies on populations exposed to fires and combustion products. Each study is discussed below including relevant results. Given the large number of studies with risk estimates for many different cancer sites, results are also summarized by cancer site in Table 6-2 at the end of this section.
Cancer in Firefighters
The objective of these studies was to examine whether or not employment as a fire fighter increases the risk of cancer. Most of the studies are retrospective cohort mortality studies of firefighters and present results for specific cancers as SMRs.
A retrospective cohort mortality study conducted by Baris et al. (2001) was particularly valuable because it quantified exposure as number of runs made by each individual firefighter. Cancer mortality among 7,789 Philadelphia firefighters was compared with the general white male U.S. population. On average, the firefighters worked for 18 years, with 26 years follow-up. There was a significant excess risk of colon cancer (SMR 1.51, 95% CI 1.18–1.93) but not other cancers. After stratification by duration of employment, cumulative number of runs, and number of runs in the first 5 years of employment, there were no positive exposure–response trends for any outcome. Stratification showed significantly increased risks of certain cancers for those employed 9 years or less (all cancers, colon, pancreas, lung, prostate), or more than 20 years (colon, kidney, multiple myeloma); those employed at engine companies (all cancers, buccal cavity and pharynx, colon, multiple myeloma) or ladder companies (leukemia), but not at engine and ladder companies; those first hired before 1935 (buccal cavity and pharynx), between 1935 and 1944 (all cancers, colon, kidney, non-Hodgkin’s lymphoma [NHL]) and after 1944 (colon); and those having made fewer than 3,323 runs (colon, NHL), 3,323 to 5,099 runs (colon, skin), but not for more than 5,099 runs.
Aronson et al. (1994) conducted a retrospective cohort mortality study of 5,414 firefighters in metropolitan Toronto. The authors compared the firefighter cohort’s mortality rate to that of the Ontario male population. The average time of follow-up was 21 years and the average term of employment was 20 years. There was a significant excess risk of brain and other nervous system cancers (SMR 2.01, 95% CI 1.10–3.37) based on 14 cases, and other malignant neoplasms based on 20 deaths (SMR 2.38, 95% CI 1.45–3.67) but not for other cancer sites. Other malignant neoplasms remained significant for several strata (30 or more years since first employment, less than 15 and more than 30 years of employment, and both age strata [less than 60 years or 60 or more years]) whereas brain and other nervous system cancers were not significantly elevated after stratification.
Bates et al. (2007) analyzed 804,107 male cancer cases from the California Cancer Registry diagnosed from 1988–2003. Firefighters (3,659 cases) were compared to other registrants with adjustments for age, year of diagnosis, ethnicity, and socioeconomic status; the analysis to was restricted to those aged 21–80 years old at diagnosis. Increased risks were reported for testicular cancer (OR 1.54; 95% CI 1.18–2.02), melanoma (OR 1.50; 95% CI 1.33–1.70), brain cancer (OR 1.35, 95% CI 1.06–1.72), prostate cancer (OR 1.22, 95% CI 1.12–1.33), and esophageal cancer (OR 1.48; 95% CI 1.14–1.91). Disease misclassification is an issue because the occupation and industry fields in the registry were self-reported and sometimes were blank, some registrants might have been volunteer firemen, and no employment duration or other way to quantify exposure was available.
Beaumont et al. (1991) conducted a retrospective cohort mortality study of 3,066 firefighters employed in San Francisco, California, between 1940 and 1970. The authors used the U.S. white male population as the reference population. Decreased risk was found for prostate cancer (SMR 0.38, 95% CI 0.16–0.75). There was a significant increased risk for esophageal cancer (SMR 2.04, 95% CI: 1.05–3.57), however, the other cancers were all nonsignificant. There was no adjustment for smoking or alcohol.
Demers et al. (1992b) studied the mortality of 4,546 men employed as firefighters in Seattle and Tacoma, Washington, and Portland, Oregon. Mortality rates in the study population were compared with the national mortality rates for U.S. males. There was no evidence of excess risk of overall mortality from cancer except for a significant increase in cancer mortality from brain tumors (SMR 2.09, 95% CI 1.3–3.2). Younger firefighters (< 40 years of age) appeared to have an excess risk of brain cancer (SMR 3.75, 95% CI 1.2–8.7). The risk of lymphatic and haematopoetic cancers was greatest for men with at least 30 years of employment exposure (SMR 2.05, 95% CI 1.1–3.6), especially for leukemia (SMR 2.60, 95% CI 1.05–4). Demers et al. (1994) conducted a later study of cancer incidence in firefighters that was limited to Seattle and Tacoma, Washington, using tumor registry data.
Duration of active duty was assignable for Seattle firefighters and used as a surrogate measure of cumulative exposure to combustion products from fires; no exposure was assigned for years spent in administrative duties or support services. Total years of employment had to be used for Tacoma firefighters because records identifying the start and end dates of specific duties were not available for all of them. The study population included 2,447 firefighters and was followed from 1974 to 1989. The cancer incidence in this firefighter population was compared with local cancer incidence rates, and with incidence in 1,878 policemen from the same cities. Compared with local rates, firefighters had an elevated rate of prostate cancer (standardized incidence ratio [SIR] 1.5, 95% CI 1.1–1.7), but no significant risks were observed for other cancers. Compared to policemen, no cancers were significantly elevated among firefighters.
Guidotti et al. (1993) conducted a retrospective cohort mortality study of 3,328 firefighters employed between 1927 and 1987 in Edmonton and Calgary, Alberta. An exposure opportunity index term, reflecting estimates of the relative time spent in close proximity to fires by job classification, was used to refine exposure data based on years of service. The authors found a significant increase for all cancers combined (SMR 1.27, 95% CI 1.02–1.55), but no excess risk for any specific cancer.
Using Massachusetts Cancer Registry data from 1986-2003, Kang et al. (2008) reported positive associations for brain cancer (standardized mortality odds ratio [SMOR] 1.90, 95% CI 1.10–3.26) and colon cancer (SMOR 1.36, 95% CI 1.04–1.79) in firefighters compared with police officers, adjusted for age and smoking status. No significant increases in mortality were seen for bladder cancer, kidney cancer, and Hodgkin’s lymphoma in firefighters, nor was there a significant association for cancer mortality in firefighters compared with all other occupations. The registry contained 258,964 eligible cancer cases, including 2,125 firefighters. This registry was previously analyzed by Sama et al. (1990), who reported excess age-adjusted ORs for melanoma (SMOR 2.92, 95% CI 1.70–5.03) and bladder cancer (SMOR 1.59, 95% CI 1.02–2.50) in firefighters compared to the rest of the state. Using policemen as the reference group, bladder cancer (SMOR 2.11, 95% CI 1.07–4.14) and NHL (SMOR 3.27, 95% CI 1.19–8.98) were elevated in firefighters but melanoma was not, although it remained significantly elevated among 55–74 year olds. Smoking patterns were compared between firefighters, policemen, and other Massachusetts males, but the SMORs were not adjusted for smoking.
Tornling et al. (1994) conducted a study of cancer incidence and mortality in firefighters in Stockholm, Sweden. An index of the number of fires fought was calculated for each individual. There were no significant increases in cancer-specific mortality, although there was some evidence for associations with brain and stomach cancers. The most highly exposed subgroup (> 1,000 fires fought) had a significant increase in brain cancer mortality (SMR 4.96, CI 1.35–12.70) based on four cases. The excess was not significant for brain cancer incidence in this subgroup (SIR 2.01, CI 0.40–5.88) based on three cases. Stomach cancer incidence was elevated overall (SIR 1.92; 95% CI 1.14–3.04). In this study, the category of high number of runs would be considered low in the Philadelphia firefighters study of Baris et al. (2001); thus, this cohort had relatively low exposure.
Vena and Fiedler (1987) conducted a retrospective cohort study of 1,867 white male firefighters in Buffalo, New York. The firefighter cohort’s mortality experience was compared with that of the U.S. population of white men and also presented SMRs by duration of employment. There were elevated SMRs for colon cancer (SMR 1.83, 95% CI 1.05–2.97), and bladder cancer (SMR 2.86, 95%CI 1.30–5.40). In the subgroup of firefighters employed more than 40 years, the SMRs increased to 4.71 and 5.71, both significant, for colon and bladder cancer, respectively.
Several other cohort studies on cancer incidence and mortality found no increased risk of cancer among firefighters. Bates et al. (2001) reported no increase in the incidence of any specific cancer site or for all cancers combined among 4,305 firefighters in New Zealand from 1977 to 1995 (1996 for cancer) except for testicular cancer (SIR 2.97, 95% CI 1.3–5.9) between 1990 and 1996, and no increased cancer mortality for any site from 1977 to 1995. After 14 years of follow-up of Parisian firefighters, Deschamps et al. (1995) found nonsignificant excess mortality for a number of outcomes including genitourinary cancer (SMR 3.29), digestive cancer (SMR 1.14), and respiratory cancer (SMR 1.12). Among male firefighters in Seattle employed for at least 1 year between 1945 and 1980, Heyer et al. (1990) found cancer mortality to be similar to the general U.S. white male population.
However, for those over 65 years of age, the SMR was 1.77 (95% CI 1.05–2.79); for those exposed for 30 years or more, the SMR for leukemia was 5.03 (95% CI 1.04–14.7) and 9.89 (95% CI 1.20–35.71) for other lymphatic and hematopoietic cancers. Ma et al. (2006) investigated incident cancer cases among 36,813 firefighters in Florida from 1981–1999 compared with the state’s general population. After adjusting for age and calendar year, significantly elevated risks were seen in men for bladder cancer (SIR 1.29, 95% CI 1.01–1.62), thyroid cancer (SIR 1.77, 95% 1.08–2.76), and testicular cancer (SIR 1.6, 95% CI 1.20–2.09). Among women, increases were reported for thyroid cancer (SIR 3.97, 95% CI 1.45–8.65) and Hodgkin’s disease (SIR 6.25, 95% CI 1.26–18.3). For male firefighters, significantly decreased risks were found for buccal cancers; digestive cancers, specifically stomach cancer; respiratory cancers, specifically lung cancer; and lymphopoietic cancers.
Using the 27 state National Occupational Mortality Surveillance database from 1984–1990, Burnett et al. (1994) found an elevated PMR for all cancers combined (1.10, 95% CI 1.06–1.14) and for those cases who died before 65 years of age the PMR was 1.12 (95% CI 1.04–1.21)among those ever employed as firefighters. For all CNS cancer deaths, the PMR was 1.03 (95% CI 0.73–1.41) and for those who died before age 65, the PMR was 0.85 (95% CI 0.52–1.34). The strength of this study is the large numbers of cancer deaths in the cohort. A related study, reported by Ma et al. (1998) used a database overlapping that of Burnett et al. (1994) to study racial differences in susceptibility to cancer among firefighters using death certificates from 24 states. An increase of CNS cancer deaths was seen for black firefighters (MOR 6.9, 95% CI 3.0–16.0) but not white firefighters. The overlap between the two studies precludes their consideration as independent investigations of CNS cancer in the white population.
Carozza et al. (2000) conducted and Krishnan et al. (2003) later expanded a population-based case control study on glioma incidence in the San Francisco bay area. The job histories of 476 (Carozza et al. 2000) and 879 (Krishnan et al. 2003) gliomas cases were identified. Both studies found “suggestive (but not significant) evidence” of higher risk of gliomas among firefighters.
The following studies lacked adequate power to identify a relationship between cancer and occupation as a firefighter. Elci et al. (2003) examined job histories of 1,354 male lung cancer cases in a large cancer therapy center in Marmara, Turkey. They found “strong evidence” of increased risk of lung cancer among firefighters, but adjustment for smoking was by smoking status (ever/never) only. Firth et al. (1996) conducted a retrospective study assessing all cancers combined and cancer-specific incidence in males by occupation in a population in New Zealand. They also found “strong evidence” of increased risk for cancer of the larynx among firefighters based on three and four cases of laryngeal cancer observed for firefighters ages 15–54 and 15–64, respectively, but there was no adjustment for smoking.
Several reviews and meta-analyses have assessed cancer risk among firefighters. A meta-analysis conducted by Howe and Burch (1990) concluded there was no increased risk of overall cancer, lung cancer, or colon cancer, but the pooled risk estimates were significantly elevated for brain cancer and multiple myeloma, indicating the possibility of an association. While the pooled risk estimate was significantly elevated for melanoma, the authors did not believe the evidence supported a causal association. To address the accumulating body of literature since the Howe and Burch publication, LeMasters et al. (2006) conducted a meta-analysis of 28 studies of firefighters for selected cancers to determine probable, possible, or unlikely risks. The likelihood of cancer risks for multiple myeloma, NHL, and prostate cancer were determined to be probable while cancers of the testes, skin, malignant melanoma, brain, rectum, buccal cavity and pharynx, stomach, colon and leukemia were classified as possible. Another meta-analysis of 16 studies by Youakim (2006) found significantly increased risks for kidney cancer, NHL mortality, and bladder cancer incidence. Furthermore, among studies having duration of employment information, significantly increased risks were found for mortality from kidney cancer with more than 20 years of employment; brain cancer, colon cancer, and leukemia with more than 30 years of employment; and bladder cancer with more than 40 years of employment as a firefighter.
Three reviews provide very different interpretations of cancer risk among firefighters. In the most recent review, Haas et al. (2003) reviewed 17 studies and found that there was no evidence of an association between employment as a firefighter and cancer mortality; however, the authors noted that consistently elevated rates of brain cancer warrant further investigation. In contrast, Golden et al. (1995) reviewed 19 studies and concluded that firefighters are at increased risk of leukemia, NHL, multiple myeloma, brain cancer, and bladder cancer with weak evidence supporting risks of rectal cancer, colon cancer, stomach cancer, prostate cancer, and melanoma.
On the basis of 21 studies, Guidotti (1995) concluded there is sufficient evidence for a presumption of increased risk among firefighters for lung cancer, genitourinary cancers, and colon and rectal cancers. Associations for brain cancer, and lymphatic and hematopoietic cancers are less clear.
In 2010, the International Agency for Research on Cancer (IARC) released a monograph including an assessment of the carcinogenicity of firefighting as an occupation. After a review of 42 epidemiologic studies and meta-analyses, IARC found increased risks for testicular cancer, prostate cancer, and NHL. The assessment concluded that “occupational exposure as a firefighter is possibly carcinogenic to humans (Group 2B),” based on “limited evidence in humans” (IARC 2010).
Cancer in Incinerator Workers and Surrounding Communities
The committee reviewed several community-based studies of cancer incidence in populations living near municipal solid waste incinerators. In these studies, exposure is measured as the distance between the place of residence and the incinerator, or as area-level dioxin concentrations at ground level estimated from air dispersion models. In the community studies, the focus is primarily on whether cancer rates are elevated in populations that live within a specified distance (radius) of an incinerator.
No key studies describing cancer associated with incinerators were identified by the committee.
Increasing distance from an incinerator is generally associated with a decreasing risk of cancer; however, cancer risks are not necessarily elevated nearest the incinerator, as demonstrated by the following studies. Elliott et al. (1996) conducted a retrospective study of cancer incidence in a population of over 14 million people living near 72 solid waste incinerators in Great Britain to investigate whether cancer incidence was associated with exposure to combustion products from the incinerators. There was a significant (p < 0.05) decline in cancer incidence associated with increasing distance from the incinerators for all cancers, as well as stomach, colorectal, liver, and lung cancer after adjustment for age, sex, and geographic region. No associations were seen for nasal and nasopharyngeal, larynx, connective tissue, or lymphatic and hematopoietic cancers. In a population-based case-control study of lung cancer, Biggeri et al. (1996) measured distance from four sources of exposure—a shipyard, iron foundry, incinerator, and the center of the city of Trieste, Italy. There were 755 histologically confirmed cases of lung cancer in men. Controls were matched by age and month of death. After adjusting for age, smoking habit, occupational exposure, and levels of PM, the excess relative risk (6.7 at the incinerator) declined with increasing distance. In a small community-based mortality study in Rome, Michelozzi et al. (1998) found no association between proximity to a waste incinerator and all cancers combined or most specific cancers after adjusting for age, gender, and socioeconomic status.
In a French ecologic study, a significant association was found between living near an incinerator, and soft-tissue sarcoma (STS) and NHL (Viel et al. 2000). Highly significant clusters for both STS and NHL (p < 0.05) were observed in the area around the municipal solid waste incinerator. A population-based case-control study confirmed an increased NHL risk (OR 2.3, 95% CI 1.4–3.8) for individuals living in the area with the highest dioxin concentration compared with those in the area with the lowest concentration (Floret et al. 2003). A follow-up study on a larger geographical area in France, found evidence of an association between dioxin exposure from a waste incinerator and increased risk of NHL (p = 0.04) after controlling for geographic area, industrial pollution, years of polluting industry, and population density (Viel et al. 2008).
One review examined reproductive effects, respiratory effects, and cancer in residential areas around incinerators and mortality and biomarkers among incinerator workers (Hu and Shy 2001). The authors report inconclusive findings for cancer. Generally these occupational studies are hampered by low statistical power, and the residential studies must account for multiple sources of exposure to potential carcinogens.
The committee also reviewed studies on long-term health outcomes for incinerator workers. Gustavsson et al.
(1993) conducted a retrospective cohort study of 5,542 chimney sweeps, 176 incinerator workers, 296 gas workers, and 695 bus garage workers. In the small cohort of incinerator workers, the SMR for esophageal cancer was 1.50, based on one case. Comba et al. (2003) conducted a case-control study in Mantua, Italy, and found a significant increase in risk of STS associated with living within 2 km of an industrial waste incinerator, after controlling for age and gender. However, when stratified by residential distance from the incinerator, five cases lived within 2 km of the incinerator (OR 31.4, 95% 5.6–176.1), but no other distances showed an increase in STS risk. A larger case-control study, by Zambon et al. (2007) of STS and residential history in a large area with 10 municipal solid waste incinerators in Veneto, Italy, found a significant increase in the risk of sarcoma on the basis of both the level and the length of modeled exposure to dioxin-like substances. Among the 172 cases and 405 controls, those with the longest and highest exposure had the highest sarcoma risk (OR 3.30, 95% CI 1.24–8.76). No adjustments were made for socioeconomic status or other potential confounders.
Cancer in Gulf War Veterans Exposed to Oil-Well–Fire Smoke
The IOM has previously evaluated the scientific literature on associations between illness and exposure to toxic agents associated with Gulf War service. Of particular interest to the committee is the IOM’s previous review of Gulf War studies of veterans exposed to smoke from oil-well fires. The current committee did not review the studies below; rather, it relied on the assessments of the earlier IOM committees who have examined the evidence and weighed the health effects literature, including cancer, related to this exposure (IOM 2005, 2006, 2010). Two assessments of brain cancer and one of respiratory cancer were considered relevant to this report.
Bullman et al. (2005) explored the relationship between estimated exposure to sarin gas during chemical munitions destruction at Khamisiyah, Iraq, in 1991 with cause-specific mortality of Gulf War veterans through December 31, 2000. Using the DoD’s 2000 sarin plume exposure model, 100,487 military personnel were identified as potentially exposed and 224,980 similarly deployed military personnel were considered unexposed. The study found an increased risk of brain cancer deaths in the exposed population (RR 1.94, 95% CI 1.12–3.34; 25 exposed cases vs. 27 unexposed cases), and there was a suggestion of a dose-response relationship with increased risk among those who were considered exposed for 2 days (6 cases) relative to 1 day (19 cases) (RR 3.26, 95% CI 1.33–7.96 and RR 1.72, 95% CI 0.95–3.10, respectively). The authors also discussed modeling exposure to smoke from oil-well fires as a confounder, and the effect estimates for exposure to Khamisiyah nerve agents remained elevated. There was no significant elevation in risk associated with exposure to oil-well fires as a main effect. Because brain cancer likely has a latent period of 10–20 years and Bullman et al. (2005) had fewer than 9 years of follow-up, it was concluded that additional follow-up is needed to draw any definitive conclusions concerning the association between exposure to oil-well fire smoke and the development of brain cancer.
Studying a broader cohort of military personnel that included the brain cancer cases discussed by Bullman et al. (2005), Barth et al. (2009) identified 144 brain cancer deaths among 621,902 Gulf War deployed veterans and 228 brain cancer deaths among 746,248 nondeployed veterans followed through 2004. There were 123,478 veterans exposed to oil-well–fire smoke based on a definition of exposure to 0.26 mg/m3 or more of total suspended particulates for at least 1 day. Smoke exposure and brain cancer risk was modeled with and without modeled exposure to nerve agents (both as exposed vs. not exposed) while controlling for age, sex, race, and unit type. Without nerve agent exposure, the relative risk for brain cancer associated with oil-well–fire smoke exposure was 1.67 (95% CI 1.05–2.65) and 1.81 (95% CI 1.00–3.27) when modeled with 2 or more days of nerve agent exposure (IOM 2010).
The Gulf War and Health report on combustion products (IOM 2005) discussed one study (Smith et al. 2002) that assessed respiratory cancer in Gulf War veterans exposed to smoke from oil-well fires.4 The report stated:
The study population consisted of 405,142 regular active-duty U.S. military personnel who were in the gulf region during the Kuwaiti oil-well fires. Hospitalization records were examined from DoD military treatment facilities from August 1, 1991, until hospitalization, separation from active-duty service, or July 31, 1999. Modeling was used to estimate troop exposure to oil-well fire smoke. The risk of malignant neoplasms of the respiratory and intrathoracic organs was modestly increased in the exposed group, but the CI included the null (adjusted RR 1.10, 95% CI 0.56–2.17). The relatively short observation period (8 years) is a limitation of this study for assessing cancer risk.
4The following text was excerpted from IOM (2005).
Cancer in OEF/OIF Veterans Exposed to Burn Pits
No epidemiologic investigations of cancer outcomes among OEF/OIF veterans specifically exposed to burn pits were available to the committee. However, accounts of cancer presumed to be attributable to burn pit emission have been described by the popular press (Risen 2010).
A few cancer sites in particular came to the committee’s attention. Brain, colon, and testicular cancer were reported at increased risks in some studies. The committee carefully considered the evidence for an association between combustion products and those cancers in firefighters, incinerator workers, and Gulf War soldiers.
There were two key cohort studies that reported positive and significant results for brain cancer and occupational exposure. In a large study of firefighters in four cities in Washington state, Demers et al. (1992b) found an excess risk of brain cancer (SMR 2.09, 95% CI 1.3–3.2). The SMR was higher (3.75, (95% CI 1.2–8.8) among firefighters less than 40 years of age, but there were no trends with duration of employment, and results were not corroborated later by Demers et al. (1994). Tornling et al. (1994) found an SMR for brain cancer of 4.96 (95% CI 1.35–12.70) based on four cases in a cohort mortality study of Swedish firefighters who had fought more than 1,000 fires and after more than 30 years of latency, but for the total cohort the SMR was 2.79 (95% CI 0.91–6.51). There were also two key registry-based case-control studies that found significant positive associations for brain cancer. Bates et al. (2007) reported an OR of 1.35 (95% CI 1.06–1.72) for firefighters relative to other occupations, based on an alternative control group selected from cases of all other cancers excluding several specific sites. Kang et al. (2008) found an SMOR of 1.90 (95% CI 1.1–2.36) using policemen as the reference group. The largest cohort study of firefighters (Baris et al. 2001), however, found no excess risk of brain cancer in firefighters. The overall SMR of 0.61 for brain cancer was based on eight cases, and there were no trends with increasing number of runs or duration of employment. In summary, there are two cohort studies (Demers et al. 1992b; Tornling et al. 1994) and two registry-based case-control studies (Bates et al. 2007; Kang et al. 2008) with elevated risk estimates for brain cancer in firefighters, all with several limitations. The largest cohort study, and the only one with a quantitative exposure assessment based on number of runs, is negative.
Evidence for colon cancer is mixed. The strongest key study (Baris et al. 2001) reported a significantly increased SMR for colon cancer of 1.51(95% CI 1.18–1.93) as did Elliott et al. (1996) (SMR = 1.04, 95% CI 1.02–1.06), Kang et al. (2008) (SMOR = 1.36, 95% CI 1.04–1.79), and Vena and Fiedler (1987) (SMR = 1.83, 95% CI 1.05–2.97). Elevated but not significant risks were reported by Demers et al. (1994) (IDR = 1.3, 95% CI 0.6–1.3) and Giudotti (1993) (SMR = 1.61, 95% CI 0.88–2.71). Several other key studies, however, found no evidence of excess risk.
Several studies reported significant risks of testicular cancer among firefighters. Three of the four key studies were positive: Bates et al. (2007) found an OR of 1.54 (95% CI 1.18–2.02), Kang et al. (2008) reported an SMOR of 1.53 (95% CI 0.75–3.14), and Aronson reported an SMR of 2.52 (95% CI 0.52–7.37), but Beaumont et al. (1991) found an SMR of 0.40 (95% CI 0.18–0.77). One supporting study by Ma et al. (2006) has an SIR for testicular cancer of 1.6 (95% CI 1.20–2.09). Similarly inconsistent significant results were reported for prostate cancer. Three key studies of disease risks among firemen reported significantly different risks than the selected control populations. Bates et al. (2007) reported an OR of 1.22 (95% CI 1.12–1.33); Beaumont et al. (1991) reported a SMR of 0.38 (95% CI 0.16–0.75); and Demers et al. (1994) reported a SIR of 1.4 (95% CI 1.1–1.7)
In summary, a review of the firefighter literature on specific cancer risks is generally inconsistent. Although there is some evidence of a positive association between firefighting and cancer of the brain, testes, and colon, it does not rise to the level of limited/suggestive for any particular cancer in light of the major study design constraints noted above. Even the best studies are limited by inadequate exposure assessment and the inappropriate selection of the general population as the reference group. Though several key studies included internal exposure-response analyses, none of these results were positive for any cancer.
The studies of firefighters, incinerator workers, and communities near incinerators do not show consistent increased risks for any specific cancer. While a few studies reported increased risks of brain, testicular, and prostate cancer, there is a lack of evidence for exposure-response relationships (based on duration of employment or number of fires fought); thus, the studies cannot be directly linked to exposure to combustion products. In the absence of
TABLE 6-2 Risk Estimates by Cancer Sitea
|Study||Study Type||Population||Risk Estimate (95% CI)|
|Aronson et al. 1994||K||Firefighters||SMR 1.05 (0.91–1.20)|
|Baris et al. 2001||K||Firefighters||SMR 1.10 (1.00–1.20)|
|Beaumont et al. 1991||K||Firefighters||SMR 0.95 (0.84–1.08)|
|Demers et al. 1994||K||Firefighters||SIR 1.1 (0.9–1.2)|
|Demers et al. 1994||K||Firefighters||IDR 1.0 (0.8–1.3)|
|Guidotti 1993||K||Firefighters||SMR 1.27 (1.02–1.55)|
|Tornling et al. 1994||K||Firefighters||SMR 1.02 (0.88–1.25)|
|Vena and Fiedler 1987||K||Firefighters||SMR 1.09 (0.89–1.32)|
|Bates et al. 2001||S||Firefighters||SIR 0.95 (0.8–1.1)|
|Burnett et al. 1994||S||Firefighters||PMR 1.10 (1.06–1.14)|
|Deschamps et al. 1995||S||Firefighters||SMR 0.89 (0.53–1.40)|
|Heyer et al. 1990||S||Firefighters||SMR 0.96 (0.77–1.18)|
|Ma et al. 2006||S||Firefighters||SIR 0.84 (0.79–0.90)|
|Elliott et al. 1996||S||Incinerator communities||SMR 1.04 (1.03–1.04)|
|Michelozzi et al. 1998||S||Incinerator communities||SMR 0.88 (0.60–1.26)|
|Gustavsson et al. 1989||S||Incinerator workers||SMR 1.07 (0.67–1.62)|
|Bullman et al. 2005||Gulf War||RR 0.97 (0.82–1.16)|
|Smith et al. 2002||Gulf War||RR 0.93 (p > 0.05)|
|Oral and Pharynx|
|Baris et al. 2001||K||Firefighters||SMR 1.36 (0.87–2.14)|
|Beaumont et al. 1991||K||Firefighters||SMR 1.43 (0.71–2.57)|
|Demers et al. 1994||K||Firefighters||SIR 1.1 (0.6–2.0)|
|Demers et al. 1994||K||Firefighters||IDR 0.8 (0.3–1.9)|
|Guidotti 1993||K||Firefighters||SMR 1.14 (0.14–4.10)|
|Kang et al. 2008||K||Firefighters||SMOR 0.72 (0.37–1.41)|
|Ma et al. 2006||S||Firefighters||SIR 0.67 (0.47–0.91)|
|Beaumont et al. 1991||K||Firefighters||SMR 6.17 (0.75–22.29)|
|Kang et al. 2008||K||Firefighters||SMOR 1.10 (0.24–5.06)|
|Beaumont et al. 1991||K||Firefighters||SMR 1.06 (0.13–3.86)|
|Aronson et al. 1994||K||Firefighters||SMR 1.39 (0.38–3.57)|
|Beaumont et al. 1991||K||Firefighters||SMR 1.17 (0.32–3.00)|
|Kang et al. 2008||K||Firefighters||SMOR 1.17 (0.19–7.17)|
|Deschamps et al. 1995||S||Firefighters||SMR 0.81 (0.10–2.93)|
|Beaumont et al. 1991||K||Firefighters||SMR 1 .27 (1.04–1.55)|
|Vena and Fiedler 1987||K||Firefighters||SMR 1.38 (0.98–1.89)|
|Deschamps et al. 1995||S||Firefighters||SMR 1.14 (0.37–2.66)|
|Heyer et al. 1990||S||Firefighters||SMR 1.06 (0.71–1.52)|
|Ma et al. 2006||S||Firefighters||SIR 0.76 (0.65–0.89)|
|Aronson et al. 1994||K||Firefighters||SMR 0.40 (0.05–1.43)|
|Baris et al. 2001||K||Firefighters||SMR 0.56 (0.25–1.24)|
|Bates et al. 2007||K||Firefighters||OR 1.48 (1.14–1.91)|
|Beaumont et al. 1991||K||Firefighters||SMR 2.04 (1.05–3.57)|
|Demers et al. 1994||K||Firefighters||SIR 1.3 (0.4–3.3)|
|Kang et al. 2008||K||Firefighters||SMOR 0.93 (0.61–1.41)|
|Vena and Fiedler 1987||K||Firefighters||SMR 1.34 (0.27–3.91)|
|Bates et al. 2001||S||Firefighters||SIR 1.67 (0.3–4.9)|
|Study||Study Type||Population||Risk Estimate (95% CI)|
|Heyer et al. 1990||S||Firefighters||SMR 0.44 (0.01–2.50)|
|Ma et al. 2006||S||Firefighters||SIR 0.62 (0.31–1.11)|
|Gustavsson et al. 1993||S||Incinerator workers||SMR 1.50 (0.04–8.34)|
|Aronson et al. 1994||K||Firefighters||SMR 0.51 (0.20–1.05)|
|Baris et al. 2001||K||Firefighters||SMR 0.90 (0.61–1.35)|
|Bates et al. 2007||K||Firefighters||OR 0.80 (0.61–1.07)|
|Beaumont et al. 1991||K||Firefighters||SMR 1.31 (0.82–1.99)|
|Demers et al. 1994||K||Firefighters||SIR 1.4 (0.6–2.7)|
|Demers et al. 1994||K||Firefighters||IDR 0.4 (0.1–1.2)|
|Guidotti 1993||K||Firefighters||SMR 0.81 (0.30–1.76)|
|Kang et al. 2008||K||Firefighters||SMOR 0.83 (0.53–1.29)|
|Tornling et al. 1994||K||Firefighters||SMR 1.21 (0.62–2.11)|
|Vena and Fiedler 1987||K||Firefighters||SMR 1.19 (0.48–2.46)|
|Bates et al. 2001||S||Firefighters||SIR 0.76 (0.2–2.2)|
|Heyer et al. 1990||S||Firefighters||SMR 1.13 (0.41–2.47)|
|Ma et al. 2006||S||Firefighters||SIR 0.5 (0.25–0.90)|
|Elliott et al. 1996||S||Incinerator communities||SMR 1.05 (1.03–1.08)|
|Gustavsson et al. 1989||S||Incinerator workers||SMR 1.32 (0.27–3.86)|
|Beaumont et al. 1991||K||Firefighters||SMR 0.99 (0.63–1.47)|
|Heyer et al. 1990||S||Firefighters||SMR 0.79 (0.32–1.64)|
|Aronson et al. 1994||K||Firefighters||SMR 0.60 (0.30–1.08)|
|Baris et al. 2001||K||Firefighters||SMR 1.51 (1.18–1.93)|
|Bates et al. 2007||K||Firefighters||OR 0.90 (0.79–1.03)|
|Demers et al. 1994||K||Firefighters||SIR 1.1 (0.7–1.6)|
|Demers et al. 1994||K||Firefighters||IDR 1.3 (0.6–3.0)|
|Guidotti 1993||K||Firefighters||SMR 1.61 (0.88–2.71)|
|Kang et al. 2008||K||Firefighters||SMOR 1.36 (1.04–1.79)|
|Tornling et al. 1994||K||Firefighters||SMR 0.85 (0.31–1.85)|
|Vena and Fiedler 1987||K||Firefighters||SMR 1.83 (1.05–2.97)|
|Bates et al. 2001||S||Firefighters||SIR 0.60 (0.2–1.2)|
|Ma et al. 2006||S||Firefighters||SIR 1.16 (0.92–1.45)|
|Elliott et al. 1996||S||Incinerator communities||SMR 1.04 (1.02–1.06)|
|Bullman et al. 2005||Gulf War||RR 1.17 (0.61–2.25)|
|Bates et al. 2007||K||Firefighters||OR 1.09 (0.82–1.44)|
|Aronson et al. 1994||K||Firefighters||SMR 1.71 (0.91–2.93)|
|Baris et al. 2001||K||Firefighters||SMR 0.99 (0.59–1.68)|
|Beaumont et al. 1991||K||Firefighters||SMR 1.45 (0.77–2.49)|
|Demers et al. 1994||K||Firefighters||SIR 1.0 (0.5–1.8)|
|Demers et al. 1994||K||Firefighters||IDR 1.3 (0.5–3.9)|
|Kang et al. 2008||K||Firefighters||SMOR 0.86 (0.58–1.26)|
|Tornling et al. 1994||K||Firefighters||SMR 2.07 (0.89–4.08)|
|Vena and Fiedler 1987||K||Firefighters||SMR 2.08 (0.83–4.28)|
|Bates et al. 2001||S||Firefighters||SIR 1.15 (0.5–2.2)|
|Burnett et al. 1994||S||Firefighters||PMR 1.48 (1.05–2.05)|
|Heyer et al. 1990||S||Firefighters||SMR 0.65 (0.08–2.37)|
|Ma et al. 2006||S||Firefighters||SIR 0.88 (0.56–1.32)|
|Study||Study Type||Population||Risk Estimate (95% CI)|
|Gustavsson et al. 1989||S||Incinerator workers||SMR 2.32 (0.28–8.37)|
|Aronson et al. 1994||K||Firefighters||SMR 0.84 (0.10–3.05)|
|Baris et al. 2001||K||Firefighters||SMR 0.82 (0.41–1.64)|
|Beaumont et al. 1991||K||Firefighters||SMR 1.91 (0.87–3.63)|
|Kang et al. 2008||K||Firefighters||SMOR 1.15 (0.55–2.41)|
|Tornling et al. 1994||K||Firefighters||SMR 1.49 (0.41–3.81)|
|Vena and Fiedler 1987||K||Firefighters||SMR 0.98 (0.11–3.52)|
|Ma et al. 2006||S||Firefighters||SIR 0.74 (0.32–1.46)|
|Elliott et al. 1996||S||Incinerator communities||SMR 1.13 (1.05–1.22)|
|Aronson et al. 1994||K||Firefighters||SMR 1.40 (0.77–2.35)|
|Baris et al. 2001||K||Firefighters||SMR 0.96 (0.64–1.44)|
|Bates et al. 2007||K||Firefighters||OR 0.90 (0.70–1.17)|
|Beaumont et al. 1991||K||Firefighters||SMR 1.25 (0.73–2.00)|
|Demers et al. 1994||K||Firefighters||SIR 1.1 (0.4–2.3)|
|Demers et al. 1994||K||Firefighters||IDR 1,1 (0.3–5.5)|
|Guidotti 1993||K||Firefighters||SMR 1.55 (0.50–3.62)|
|Kang et al. 2008||K||Firefighters||SMOR 0.86 (0.53–1.40)|
|Tornling et al. 1994||K||Firefighters||SMR 0.84 (0.27–1.96)|
|Vena and Fiedler 1987||K||Firefighters||SMR 0.38 (0.04–1.36)|
|Bates et al. 2001||S||Firefighters||SIR 1.28 (0.3–3.7)|
|Ma et al. 2006||S||Firefighters||SIR 0.57 (0.30–1.10)|
|Bullman et al. 2005||Gulf War||RR 0.82 (0.39–1.73)|
|Beaumont et al. 1991||K||Firefighters||SMR 0.83 (0.64–1.06)|
|Vena and Fiedler 1987||K||Firefighters||SMR 0.94 (0.62–1.36)|
|Deschamps et al. 1995||S||Firefighters||SMR 1.12 (0.45–2.30)|
|Heyer et al. 1990||S||Firefighters||SMR 1.01 (0.65–1.34)|
|Ma et al. 2006||S||Firefighters||SIR 0.67 (0.57–0.78)|
|Demers et al. 1994||K||Firefighters||SIR 2.2 (0.1–12.4)|
|Aronson et al. 1994||K||Firefighters||SMR 0.37 (0.01–2.06)|
|Baris et al. 2001||K||Firefighters||SMR 0.75 (0.31–1.81)|
|Beaumont et al. 1991||K||Firefighters||SMR 0.80 (0.17–2.35)|
|Demers et al. 1994||K||Firefighters||SIR 1.0 (0.3–2.3)|
|Demers et al. 1994||K||Firefighters||IDR 0.8 (0.2–3.5)|
|Kang et al. 2008||K||Firefighters||SMOR 0.66 (0.39–1.10)|
|Firth et al. 1996||S||Firefighters||SIR 10.74 (2.79–27.76)|
|Ma et al. 2006||S||Firefighters||SIR 0.73 (0.44–1.12)|
|Michelozzi et al. 1998||S||Incinerator communities||SMR 2.36 (0.27–8.00)|
|Aronson et al. 1994||K||Firefighters||SMR 0.95 (0.71 –1.24)|
|Baris et al. 2001||K||Firefighters||SMR 1.13 (0.97–1.32)|
|Bates et al. 2007||K||Firefighters||OR 0.98 (0.88–1.09)|
|Beaumont et al. 1991||K||Firefighters||SMR 0.84 (0.64–1.08)|
|Demers et al. 1994||K||Firefighters||IDR 1.1 (0.6–1.9)|
|Demers et al. 1994||K||Firefighters||SIR 1.0 (0.7–1.3)|
|Guidotti 1993||K||Firefighters||SMR 1.42 (0.91–2.11)|
|Kang et al. 2008||K||Firefighters||SMOR 1.02 (0.79–1.31)|
|Study||Study Type||Population||Risk Estimate (95% CI)|
|Tornling et al. 1994||K||Firefighters||SMR 0.90 (0.53–1.42)|
|Bates et al. 2001||S||Firefighters||SIR 1.14 (0.7–1.8)|
|Burnett et al. 1994||S||Firefighters||PMR 1.02 (0.94–1.11)|
|Elci et al. 2003||S||Firefighters||OR 6.8 (1.3–37.4)|
|Firth et al. 1996||S||Firefighters||SIR 1.65 (0.60–3.62)|
|Heyer et al. 1990||S||Firefighters||SMR 0.97 (0.65–1.39)|
|Ma et al. 2006||S||Firefighters||SIR 0.65 (0.54–0.78)|
|Biggeri et al. 1996||S||Incinerator communities||Excess 1.48 (p = 0.0937) risk|
|Elliott et al. 1996||S||Incinerator communities||SMR 1.08 (1.07–1.09)|
|Michelozzi et al. 1998||S||Incinerator communities||SMR 0.95 (0.48–1.69)|
|Gustavsson et al. 1989||S||Incinerator workers||SMR 1.97 (0.90–3.74)|
|Bullman et al. 2005||Gulf War||RR 0.72 (0.47–1.10)|
|Ma et al. 2006||S||Firefighters||SIR 1.02 (0.27–2.61)|
|Soft Tissue Sarcoma|
|Kang et al. 2008||K||Firefighters||SMOR 1.05 (0.46–2.37)|
|Ma et al. 2006||S||Firefighters||SIR 1 (0.55–1.69)|
|Elliott et al. 1996||S||Incinerator communities||SMR 1.03 (0.94–1.13)|
|Viel et al. 2000||S||Incinerator communities||SIR 1.44 (p = 0.004)|
|Comba et al. 2003||S||Incinerator workers||OR 31.4 (5.6–176.1)|
|Zambon et al. 2007||S||Incinerator workers||OR 3.30 (1.24–8.76)|
|Aronson et al. 1994||K||Firefighters||SMR 0.73 (0.09–2.63)|
|Baris et al. 2001||K||Firefighters||SMR 1.18 (0.64–2.20)|
|Bates et al. 2007||K||Firefighters||OR 1.50 (1.33–1.70)|
|Beaumont et al. 1991||K||Firefighters||SMR 1.69 (0.68–3.49)|
|Demers et al. 1994||K||Firefighters||IDR 1.0 (0.4–1.8)|
|Demers et al. 1994||K||Firefighters||SIR 1.2 (0.6–2.3)|
|Guidotti 1993||K||Firefighters||SMR 0.0 (0.0–3.31)|
|Kang et al. 2008||K||Firefighters||SMOR 0.65 (0.44–0.97)|
|Bates et al. 2001||S||Firefighters||SIR 1.26 (0.8–1.9)|
|Burnett et al. 1994||S||Firefighters||PMR 1.63 (1.15–2.23)|
|Ma et al. 2006||S||Firefighters||SIR 1.17 (0.95–1.42)|
|Demers et al. 1994||K||Firefighters||SIR 2.4 (0.1–13.3)|
|Kang et al. 2008||K||Firefighters||SMOR 0.25 (0.03–2.31)|
|Ma et al. 2006||S||Firefighters||SIR 0.51 (0.06–1.84)|
|Deschamps et al. 1995||S||Firefighters||SMR 3.29 (0.40–11.88)|
|Aronson et al. 1994||K||Firefighters||SMR 1.32 (0.76–2.15)|
|Baris et al. 2001||K||Firefighters||SMR 0.96 (0.68–1.37)|
|Bates et al. 2007||K||Firefighters||OR 1.22 (1.12–1.33)|
|Beaumont et al. 1991||K||Firefighters||SMR 0.38 (0.16–0.75)|
|Demers et al. 1994||K||Firefighters||SIR 1.4 (1.1–1.7)|
|Demers et al. 1994||K||Firefighters||IDR 1.1 (0.7–1.8)|
|Guidotti 1993||K||Firefighters||SMR 1.46 (0.63–2.88)|
|Kang et al. 2008||K||Firefighters||SMOR 0.98 (0.78–1.23)|
|Tornling et al. 1994||K||Firefighters||SMR 1.21 (0.66–2.02)|
|Vena and Fiedler 1987||K||Firefighters||SMR 0.71 (0.23–1.65)|
|Bates et al. 2001||S||Firefighters||SIR 1.08 (0.5–1.9)|
|Study||Study Type||Population||Risk Estimate (95% CI)|
|Ma et al. 2006||S||Firefighters||SIR 1.1 (0.95–1.42)|
|Aronson et al. 1994||K||Firefighters||SMR 2.52 (0.52–7.37)|
|Bates et al. 2007||K||Firefighters||OR 1.54 (1.18–2.02)|
|Beaumont et al. 1991||K||Firefighters||SMR 0.40 (0.18–0.77)|
|Kang et al. 2008||K||Firefighters||SMOR 1.53 (0.75–3.14)|
|Bates et al. 2001||S||Firefighters||SIR 1.55 (0.8–2.8)|
|Ma et al. 2006||S||Firefighters||SIR 1.6 (1.20–2.09)|
|Aronson et al. 1994||K||Firefighters||SMR 1.28 (0.51–2.63)|
|Baris et al. 2001||K||Firefighters||SMR 1.25 (0.77–2.00)|
|Bates et al. 2007||K||Firefighters||OR 0.85 (0.72–1.00)|
|Beaumont et al. 1991||K||Firefighters||SMR 0.57 (0.19–1.35)|
|Beaumont et al. 1991||K||Firefighters||SMR 0.61 (0.28–1.17)|
|Demers et al. 1994||K||Firefighters||SIR 1.2 (0.7–1.9)|
|Demers et al. 1994||K||Firefighters||IDR 1.7 (0.7–4.3)|
|Guidotti 1993||K||Firefighters||SMR 3.16 (0.86–8.08)|
|Kang et al. 2008||K||Firefighters||SMOR 1.22 (0.89–1.69)|
|Vena and Fiedler 1987||K||Firefighters||SMR 2.86 (1.30–5.40)|
|Bates et al. 2001||S||Firefighters||SIR 1.14 (0.4–2.7)|
|Burnett et al. 1994||S||Firefighters||PMR 0.99 (0.70–1.37)|
|Ma et al. 2006||S||Firefighters||SIR 1.29 (1.01–1.62)|
|Elliott et al. 1996||S||Incinerator communities||SMR 1.01 (0.98–1.04)|
|Gustavsson et al. 1989||S||Incinerator workers||SMR 1.39 (0.03–7.77)|
|Aronson et al. 1994||K||Firefighters||SMR 0.43 (0.05–1.56)|
|Baris et al. 2001||K||Firefighters||SMR 1.07 (0.61–1.88)|
|Bates et al. 2007||K||Firefighters||OR 1.07 (0.87–1.31)|
|Beaumont et al. 1991||K||Firefighters||SMR 0.68 (0.19–1.74)|
|Demers et al. 1994||K||Firefighters||SIR 0.5 (0.1–1.6)|
|Demers et al. 1994||K||Firefighters||IDR 0.4 (0.1–2.1)|
|Guidotti 1993||K||Firefighters||SMR 4.14 (1.66–8.53)|
|Kang et al. 2008||K||Firefighters||SMOR 1.34 (0.90–2.01)|
|Tornling et al. 1994||K||Firefighters||SMR 1.10 (0.30–2.81)|
|Vena and Fiedler 1987||K||Firefighters||SMR 1.30 (0.26–3.80)|
|Bates et al. 2001||S||Firefighters||SIR 0.57 (0.1–2.1)|
|Burnett et al. 1994||S||Firefighters||PMR 1.44 (1.08–1.89)|
|Ma et al. 2006||S||Firefighters||SIR 0.78 (0.52–1.14)|
|Michelozzi et al. 1998||S||Incinerator communities||SMR 2.76 (0.31–9.34)|
|Brain and Nervous System|
|Aronson et al. 1994||K||Firefighters||SMR 2.01 (1.10–3.37)|
|Beaumont et al. 1991||K||Firefighters||SMR 0.81 (0.26–1.90)|
|Vena and Fiedler 1987||K||Firefighters||SMR 2.36 (0.86–5.13)|
|Burnett et al. 1994||S||Firefighters||PMR 1.03 (0.73–1.41)|
|Heyer et al. 1990||S||Firefighters||SMR 0.95 (0.26–7.89)|
|Ma et al. 2006||S||Firefighters||SIR 0.58 (0.31–0.97)|
|Demers et al. 1994||K||Firefighters||SIR 5.2 (0.6–18.8)|
|Ma et al. 2006||S||Firefighters||SIR 1.54 (0.42–3.95)|
|Study||Study Type||Population||Risk Estimate (95% CI)|
|Baris et al. 2001||K||Firefighters||SMR 0.61 (0.31–1.22)|
|Bates et al. 2007||K||Firefighters||OR 1.35 (1.06–1.72)|
|Demers et al. 1994||K||Firefighters||SIR 1.1 (0.3–2.9)|
|Demers et al. 1994||K||Firefighters||IDR 1.4 (0.2–11)|
|Guidotti 1993||K||Firefighters||SMR 1.47 (0.30–4.29)|
|Kang et al. 2008||K||Firefighters||SMOR 1.90 (1.10–3.26)|
|Tornling et al. 1994||K||Firefighters||SMR 2.79 (0.91–6.51)|
|Bates et al. 2001||S||Firefighters||SIR 1.27 (0.4–3.0)|
|Gustavsson et al. 1989||S||Incinerator workers||SMR 2.44 (0.06–13.59)|
|Barth et al. 2009||Gulf War||RR 0.90 (0.73–1.11)|
|Bullman et al. 2005||Gulf War||RR 1.94 (1.12–3.34)|
|Carrozza et al. 2000||S||Firefighters||OR 2.7 (0.3–26.1)|
|Krishnan et al. 2003||S||Firefighters||OR 5.88 (0.70–49.01)|
|Bates et al. 2007||K||Firefighters||OR 1.17 (0.82–1.67)|
|Demers et al. 1994||K||Firefighters||SIR 0.8 (0.2–4.2)|
|Kang et al. 2008||K||Firefighters||SMOR 0.71 (0.30–1.70)|
|Ma et al. 2006||S||Firefighters||SIR 1.77 (1.08–2.73)|
|Lymphatic and Hematopoietic|
|Aronson et al. 1994||K||Firefighters||SMR 0.98 (0.58–1.56)|
|Beaumont et al. 1991||K||Firefighters||SMR 0.65 (0.35–1.09)|
|Beaumont et al. 1991||K||Firefighters||SMR 0.89 (0.24–2.29)|
|Guidotti 1993||K||Firefighters||SMR 1.27 (0.61–2.33)|
|Tornling et al. 1994||K||Firefighters||SMR 0.44 (0.09–1.27)|
|Vena and Fiedler 1987||K||Firefighters||SMR 0.55 (0.18–1.29)|
|Burnett et al. 1994||S||Firefighters||PMR 1.30 (1.11–1.51)|
|Heyer et al. 1990||S||Firefighters||SMR 1.26 (0.65–2.22)|
|Ma et al. 2006||S||Firefighters||SIR 0.68 (0.54–0.85)|
|Elliott et al. 1996||S||Incinerator communities||SMR 1.01 (0.99–1.03)|
|Michelozzi et al. 1998||S||Incinerator communities||SMR 1.20 (0.24–3.37)|
|Gustavsson et al. 1989||S||Incinerator workers||SMR 1.30 (0.16–4.71)|
|Aronson et al. 1994||K||Firefighters||SMR 2.04 (0.42–5.96)|
|Demers et al. 1994||K||Firefighters||SIR 0.7 (0.0–4.1)|
|Kang et al. 2008||K||Firefighters||SMOR 1.81 (0.72–4.53)|
|Ma et al. 2006||S||Firefighters||SIR 0.77 (0.38–1.38)|
|Baris et al. 2001||K||Firefighters||SMR 1.41 (0.91–2.19)|
|Bates et al. 2007||K||Firefighters||OR 1.07 (0.90–1.26)|
|Demers et al. 1994||K||Firefighters||IDR 1.8 (0.4–13)|
|Demers et al. 1994||K||Firefighters||SIR 0.9 (0.4–1.9)|
|Kang et al. 2008||K||Firefighters||SMOR 0.77 (0.31–1.92)|
|Burnett et al. 1994||S||Firefighters||PMR 1.32 (1.02–1.67)|
|Ma et al. 2006||S||Firefighters||SIR 1.09 (0.61–1.80)|
|Elliott et al. 1996||S||Incinerator communities||SMR 1.03 (1.00–1.07)|
|Floret et al. 2003||S||Incinerator communities||OR 2.3 (1.4–3.8)|
|Michelozzi et al. 1998||S||Incinerator communities||SMR 2.51 (0.29–8.51)|
|Viel et al. 2008||S||Incinerator communities||RR 1.12 (1.002–1.251)|
|Viel et. al. 2000||S||Incinerator communities||SIR 1.27 (p = 0.00003)|
|Aronson et al. 1994||K||Firefighters||SMR 0.47 (0.01–2.59)|
|Study||Study Type||Population||Risk Estimate (95% CI)|
|Baris et al. 2001||K||Firefighters||SMR 1.68 (0.90–3.11)|
|Bates et al. 2007||K||Firefighters||OR 1.03 (0.75–1.43)|
|Demers et al. 1994||K||Firefighters||SIR 0.7 (0.1–2.6)|
|Kang et al. 2008||K||Firefighters||SMOR 0.76 (0.39–1.48)|
|Burnett et al. 1994||S||Firefighters||PMR 1.48 (1.02–2.07)|
|Aronson et al. 1994||K||Firefighters||SMR 1.20 (0.33–3.09)|
|Aronson et al. 1994||K||Firefighters||SMR 1.90 (0.52–4.88)|
|Baris et al. 2001||K||Firefighters||SMR 0.83 (0.50–1.37)|
|Bates et al. 2007||K||Firefighters||OR 1.22 (0.99–1.49)|
|Beaumont et al. 1991||K||Firefighters||SMR 0.61 (0.22–1.33)|
|Demers et al. 1994||K||Firefighters||SIR 1.0 (0.4–2.1)|
|Demers et al. 1994||K||Firefighters||IDR 0.8 (0.2–3.5)|
|Kang et al. 2008||K||Firefighters||SMOR 0.72 (0.43–1.20)|
|Bates et al. 2001||S||Firefighters||SIR 1.81 (0.5–4.6)|
|Burnett et al. 1994||S||Firefighters||PMR 1.19 (0.91–1.53)|
|Heyer et al. 1990||S||Firefighters||SMR 1.73 (0.70–3.58)|
|Ma et al. 2006||S||Firefighters||SIR 0.77 (0.47–1.19)|
|Michelozzi et al. 1998||S||Incinerator communities||SMR 0.82 (0.03–4.09)|
|Aronson et al. 1994||K||Firefighters||SMR 1.20 (0.33–3.09)|
|Beaumont et al. 1991||K||Firefighters||SMR 1.11 (0.76–1.58)|
|Deschamps et al. 1995||S||Firefighters||SMR 1.18 (0.14–4.27)|
NOTE: Risk estimates in bold italics denote significant differences in risk. K = key study; S = supporting study.
aThe risk estimates included in Table 6-2 reflect the cause-specific mortality or diagnosis for the study population as a whole. Many of these studies also include risk estimates by work duration, time since first exposure, or latency, but those data are not included here. For more detailed results, see chapter text or Appendix C.
better exposure assessment, the committee concluded there is no evidence for any one cancer site that rises above the level of inadequate/insufficient. Studies of Gulf War veterans exposed to oil-well–fire smoke also showed no cancer sites of concern, including brain cancer.
Based on a review of the epidemiologic literature, the committee concludes that there is inadequate/insufficient evidence of an association between long-term exposure to combustion products and cancer in the populations studied.
Cohort mortality studies often present SMRs for all causes of death combined as well as for specific causes of death. The all-cause SMR is an indication of how healthy the study population is in comparison to the population chosen to represent the background rates of disease. An all-cause SMR serves as a measure of the comparability of the study group with the reference population and can highlight potential biases in the study design and analysis.
All-Cause Mortality in Firefighters
Occupational cohort mortality studies comparing an employed group with the general population typically report SMRs for all causes of death combined as less than 1.0, indicating that fewer cohort members died than expected after adjusting for age, race, gender, and calendar year. One explanation for the commonly observed deficit is the healthy worker effect, a form of selection bias reflected in the better health status of workers relative to the general population (Fox and Collier 1976). The SMR for all causes of death combined can be interpreted
TABLE 6-3 All-Cause Mortality Among Firefighters
|Study||SMR (95% CI)|
|Aronson et al. 1994||0.95 (0.88–1.02)|
|Baris et al. 2001||0.96 (0.92–0.99)a|
|Beaumont et al. 1991||0.90 (0.85–0.95)a|
|Demers et al. 1992a||0.81 (0.77–0.86)a|
|Deschamps et al. 1995||0.52 (0.35–0.75)a|
|Eliopulos et al. 1984||0.80 (0.67–0.96)a|
|Guidotti 1993||0.96 (0.87–1.07)|
|Hansen 1990||0.99 (0.75–1.29)|
|Heyer et al. 1990||0.76 (0.69–0.85)a|
|Ma et al. 2005||0.57 (0.54–0.60)a|
|Tornling et al. 1994||0.82 (0.73–0.91)a|
|Vena and Fiedler 1987||0.95 (0.87–1.04)|
aSMR values in bold italics indicate a significant difference.
as a measure of the extent of the bias in a particular study (Monson 1986). There is some evidence that health worker effect bias affects chronic disease mortality such as cardiovascular, lung, and digestive diseases more than cancer (Blair et al. 1986).
Several of the studies reviewed earlier in this chapter report results for all-cause mortality. In particular, Vena and Fiedler (1987), Hansen (1990), Guidotti et al. (1993), and Aronson et al. (1994), reported SMRs of less than 1.0 with wide confidence intervals that included the null. Eight studies, Eliopulos et al. (1984), Heyer et al. (1990), Beaumont et al. (1991), Demers et al. (1992a), Tornling et al. (1994), Deschamps et al. (1995), Baris et al. (2001), and Ma et al. (2005), and found that overall mortality in firefighters was significantly lower than the reference groups. See Table 6-3 for the all-cause mortality SMRs for firefighters.
All-Cause Mortality Among Incinerator Workers and Communities Near Incinerators
One study (Gustavsson 1989) reported elevated all-cause mortality for incinerator workers compared to National Swedish mortality rates and to local rates for the greater Stockholm area (SMR 1.13, 95% CI 0.9–1.14, and SMR 0.99, 95% CI 0.79–1.22, respectively).
The committee concludes that there is insufficient/inadequate evidence to determine whether an association exists between all-cause mortality and exposure to combustion products in the populations studied.
The committee studied the epidemiologic literature on exposure to combustion products from sources believed to be relevant to the burn pit exposures at JBB and other bases with burn pits in Iraq and Afghanistan. From that epidemiologic literature, the committee concludes that further study of health effects specifically among OEF/OIF veterans is necessary. The 2010 joint services report describing several health outcomes in military personnel at bases with and without operating burn pits is a first step in addressing some of these issues but the period of follow-up is too short to detect long-term health effects in this population (AFHSC et al. 2010). Further follow-up of these populations is warranted.
The research considered in this chapter is a best attempt to use currently available information on occupational and residential exposures to combustion products to extrapolate to exposures of military personnel stationed at JBB. However, because of differences in exposure parameters, population characteristics, access to medical care, and monitoring of health, the results for firefighters, incineration workers, and people living near incinerators might not be generalizable to military personnel exposed to burn pit emissions. Furthermore, although the dif-
ficulties in determining exposure to burn pits are apparent (see Chapter 4) such assessments are critical if adverse health outcomes that might result from such exposures are to be distinguished from those that might result from deployment per se and desert environments. The committee recognizes that the risks associated with being a firefighter, incinerator worker, or living near and incinerator might not provide a comprehensive picture of the risks posed to military personnel from burn pit emissions. Nevertheless, given the lack of information on the health effects associated with such exposures, the committee believes that studies of these surrogate populations provide a reasonable approach for evaluating the long-term consequences of exposure to combustion products similar to burn pit emissions.
Based on a review of the epidemiologic literature presented in this chapter, the committee concludes that there is limited/suggestive evidence of an association between exposure to combustion products and reduced pulmonary function in the populations studied. However, there is inadequate/insufficient evidence of an association between exposure to combustion products and cancer, respiratory disease, circulatory disease, neurologic disease, and adverse reproductive and developmental outcomes in the populations studied.
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