V.  GENERAL HEALTH EFFECTS AND ISSUES ASSOCIATED WITH EXPOSURE TO PARTICULATES

A.  Background

This investigation has been complicated by the absence of medical data relating respiratory symptoms to PM levels during and after the Gulf War. This information would have been valuable not only in establishing a link between PM levels and the acute symptoms experienced by some veterans, but also for determining the potential for chronic or long-term health problems associated with these exposures. In the absence of such data, Deployment Health Support Directorate (DHSD) analysts used the medical and scientific literature to identify plausible relationships and describe symptoms that might be similar to those experienced by some veterans because of their exposure to PM. However, a search of the medical literature by DHSD analysts has not revealed any studies that specifically examine the respiratory symptoms experienced by Gulf War veterans due to PM exposures. Furthermore, many of the findings reported in the literature focus on exposure scenarios different from those experienced during the Gulf War in terms of the period of exposure, the geographic environment, and the study populations. For example, some studies in the literature focus on exposures in occupational settings and others on ambient urban environments that may have also included co-pollutants that would confound the analysis. Researchers assessed both short- and long-term exposures. Other studies focused on exposures to sensitive populations: those with pre-existing conditions, the elderly and the very young. As a result, a straightforward extrapolation between literature study results and the Gulf War experience is not appropriate. Gulf War veterans were, in general, a young, healthy population that was exposed to PM levels for a relatively short duration. Therefore, this report relates how PM may, under certain circumstances, affect one’s health, but does not prescribe expected effects in Gulf War veterans.

B.   Mechanism of Exposure

Particles of about 10 �m (PM10) or less in aerodynamic equivalent diameter are capable of reaching the alveoli (air sacks in the lung),[19] and those measuring between 0.5 and 1.0 �m aerodynamic diameter have the highest possibility of being deposited and retained in the alveoli.[20] The lower respiratory tract clearance mechanism is highly efficient and capable of completely eliminating all particles smaller than five �m as long as the airborne concentration does not exceed 10 particles per cubic centimeter. However, in environments with a much higher concentration of airborne particulates, (e.g., 1000 particles per cubic centimeter), the efficiency level of the lower respiratory tract clearance system declines to approximately 90 percent elimination.[21]

Overall, the risk of adverse health effects from inhaled particles is a function of the concentration of PM10 in the air, the duration of exposure, the penetration and deposition of particles in the regions of the respiratory tract, and the body’s biological responses to the deposited materials. These factors relate to the amount of a pollutant that actually enters the body over a specified period of time. The largest particles deposit in the air passages of the nose and sinuses (upper respiratory tract); smaller particles deposit in the large and medium bronchi (middle respiratory tract); and still smaller particles (down to 0.01 mm) reach and are retained in the gas exchange region of the lung (lower respiratory tract). Those smaller than 0.01 mm generally are not retained in large quantities, remain suspended and are eventually exhaled. Retention of particles is a function of deposition site, clearance of particles by macrophages, and particle characteristics, especially solubility. Acute effects (see Section V.C.1) of PM are related to the deposited dose of the pollutant that enters the body but, because of the body’s clearance mechanism, is not totally retained. Chronic effects (see Section V.C.2) may be related to the dose that remains in the body. Chronic effects may also arise from severe acute effects or from recurring cycles of pulmonary injury and repair.[22]

C.   Adverse Health Effects Associated with Particulate Matter Exposure

1.  Acute Effects

The scientific literature on PM epidemiology suggests an association between ambient PM exposures and various acute health outcomes. In particular, pulmonary function studies are suggestive of short-term effects resulting from ambient PM exposures. Such outcomes include hospital admissions, inflammatory response in the respiratory tract, exacerbation of asthma, and decreased lung functions.[23] A review of the findings indicates that:

  1. Sensitive populations such as individuals with asthma and other respiratory diseases, individuals with cardiovascular disease, the elderly and children are susceptible to more severe symptoms, including cough, phlegm, wheezing, shortness of breath, bronchitis, increased asthma attacks, and aggravation of lung or heart disease;
  2. Cardiovascular causes of death and hospitalization in older adults may be a component of PM-attributable mortality;
  3. PM health effects have been associated with several different PM size fractions; and
  4. Health effects may occur at different time scales for exposure to PM.[24]

Epidemiology findings indicate that risk of mortality due to lower respiratory disease (e.g., pneumonia) is increased by ambient PM exposure.[25] This may be due to exacerbation by PM of existing respiratory disease. Particulate matter may increase susceptibility to infectious disease by decreasing clearance, impairing macrophage function, or through other effects on the immune system. The findings also indicate that individuals with preexisting infectious respiratory disease (e.g., pneumonia) are at increased risk for PM effects.

Recent studies are generally consistent with regard to ambient PM associations of short-term exposures with respiratory-related hospital admissions and medical visits. The risk for adverse health effects attributable to PM that exceed those expected in a normal population fall most consistently in the range of 5 to 25 percent per 50 mg/m3 PM10 increments. Those for asthma visits and hospital admissions tend to be somewhat higher than for chronic obstructive pulmonary disease and pneumonia hospital admissions.[26] In other words, for every 50 mg/m3 increase in PM10 levels, one would expect to see a 5 to 25 percent increase in the number of emergency room visits for asthma or hospital admissions for respiratory complaints in a normal population. This population includes both healthy individuals and those susceptible to respiratory problems.

Epidemiologic findings also indicate that ambient PM exposures in the elderly are associated with increased risk for mortality and hospitalization due to cardiovascular causes. Researchers have hypothesized that cardiac arrhythmia contributes to increased mortality due to PM exposure. Thus, individuals with pre-existing cardiovascular disease(s) have been identified as a susceptible group for increased risk from ambient PM effects.[27]

Adverse health effects from acute exposures to PM may sometimes be confounded by the presence of co-pollutants such as volatile organic compounds, metals, nitrogen and sulfur containing oxides, carbon monoxide, ozone, and carbon dioxide, making it difficult to estimate that portion of risk attributable solely to respirable PM.[28] These gaseous pollutants are typically present with particulate matter and are capable of producing adverse health effects, with carbon monoxide often identified with cardiovascular effects and the others with respiratory effects.

Among 13 independent studies that included measurements of PM10 and co-pollutants, three studies reported health effects that appeared independent of co-pollutants;[29] eight reported no significant health effects after inclusion of co-pollutants;[30] and two were unclear regarding independent health effects.[31] In a recent review of the literature on airborne particles and hospital admissions for cardiovascular disease, one researcher noted that adjustments for co-pollutants consistently reduced the PM health effect.[32] Several studies appear to provide evidence for PM-related health effects independent of co-pollutant health effects. Other studies examining co-pollutants yield results showing PM effects in some studies while not in others.

In addition to inhalation exposures to PM, dermal (skin) exposures can also produce short-term, reversible symptoms. Anecdotal information received from Gulf War veterans suggests that some personnel experienced rashes, skin irritation, and scaling. Particulates containing silica in particular are associated with specific types of dermatitis and skin inflammation.[33]

2.  Chronic Effects

The recent literature contains the results of several studies that evaluate the effects of long-term PM exposure on respiratory illness, pulmonary function, cardiovascular morbidity, mortality, and cancer rates. In general, chronic respiratory illness and pulmonary function decrement studies are less numerous than acute studies, and the findings are inconclusive and inconsistent. Some studies show effects for some health endpoints (e.g., pneumonia, reduced lung function, and bronchitis) with high significant results, but other studies fail to find the same effects.[34] For example, chronic pulmonary studies, looking for latent effects, by one group of researchers showed no effect for children from airborne particle pollution.[35] In contrast, another group of researchers studying Canadian and United States' children found significant associations between pulmonary function and PM levels.[36] Temporal and spatial differences between study areas also confound results.

Results of studies conducted in urban environments provided data on the positive relationship between chronic respiratory disease and elevated long-term particulate matter levels. Study results suggest a potential long-term PM exposure effect on chronic respiratory disease.[37] Other studies report associations between PM exposures and bronchitis rates and/or lung function decrements or slowed lung function growth in children.[38]

Some researchers noted that, as PM increased in urban communities, an increase in bronchitis occurred. However, because of a high correlation between PM levels and potentially confounding factors, clear attribution of bronchitis effects to PM alone is not practical.[39]

Numerous PM epidemiology studies have implicated ambient PM levels as a likely contributor to mortality and morbidity effects, particularly among the chronically ill or elderly. For example, of particular interest with regard to PM-related effects on cause-specific mortality is a growing body of evidence linking long-term PM exposure with increased risk of lung cancer. Historical evidence includes studies of lung cancer trends, studies of occupational groups, comparisons of urban and rural populations, and case-control and cohort studies using diverse exposure metrics.[40] These studies have generally indicated an elevated risk for lung cancer relative to living in urban areas where ambient PM levels exceed the NAAQS of 50 m g/m3 (annual arithmetic mean).[41] More recent findings suggest that living in cities where the NAAQS is exceeded is associated with an elevated risk of lung cancer amounting to 10 to 15 percent above the risk in cities where the NAAQS is not exceeded.[42]

D.  Particulate Matter Components of Concern

The health effects literature has focused on PM as a single unit without respect to its individual components. Atmospheric PM occurs naturally as fine-mode and coarse-mode particles that differ in size, formation mechanisms, chemical composition, and sources. Furthermore, its composition can be expected to vary over time and space. It is difficult, therefore, to estimate the total risk of adverse health effects from exposure to PM based on the analysis of its individual component species because the components vary and the risks for each are not necessarily additive. However, a reasonable estimate of the potential risk of chronic or long-term health effects based on component analyses can be made by focusing on those components that are: 1) significant from a total mass standpoint (i.e., they represent a significant size fraction of the sample); 2) capable of inducing a physiological change or damage to lung tissue and cells; and 3) are associated with or originated from a source that potentially represents a major health concern. These factors help define the potential PM components of concern. Because silica is widespread in desert dust and highly toxic in certain forms, the emphasis of this report is on potential health effects of respirable silica exposure to servicemembers. Similarly, the widespread presence of soot from completely and partially combusted components of crude oil created concern by military health professionals for potential adverse health effects.

An occupational environment typically involves long-term exposure to silica and soot, resulting in respiratory distress and often leading to chronic effects and reduced pulmonary function. Because of the inconsistencies and uncertainties associated with the chronic health effects studies noted in the previous section, an examination of these constituents may be useful to estimate the relationship between PM exposure and potential chronic effects. In other words, could the short-term exposures experienced by US personnel to PM containing silica and soot be a source of some of the unexplained adverse health effects reported by some Gulf War veterans? Subsequent sections of this report examine this issue.

1.  Silica

The literature search indicates that researchers have studied silica exposures and associated health effects extensively in an occupational environment (e.g., among sandblasters, miners, and quarry workers). Researchers have studied the deposition of silica containing dust in the lungs of the inhabitants of the Saharan, Libyan, Negev, and Arabian Deserts. Chronic exposures have led to the development of a benign, non-progressive pneumoconiosis (disease of the lung characterized by fibrosis). This condition, sometimes referred to as Desert Lung Syndrome, differs from the occupational silicosis found in some industrial or mining settings in that it does not produce symptoms of disease and does not progress or worsen with time. The benign nature of the condition has been attributed to the difference between "old dust" and "new dust."[43] Old sand dust particles have surfaces that have been weathered or transformed over time. New dust particles are of more recent origin and are freshly fractured, sharp, with exposed new surface area.

Freshly fractured silica is more biologically reactive; that is, the relatively non-weathered surfaces of silica can cause a chemical-biological reaction with and damage to the DNA in lung tissue and thus is more likely to induce an adverse effect in living tissues and cells.[44] Exposure to freshly fractured silica may occur in a variety of occupations, including foundry work, granite work, mining and tunneling, and ceramic industry work.

Analytical data developed from samples of PM collected after the Gulf War did not differentiate between old and new dust. Although the Gulf War exposures probably involved old dust, the HRA, in determining risks associated with exposure to silica containing PM, adopts a conservative approach that assumes all silica was new or freshly fractured.[45]

In the workplace, long-term or chronic exposures to respirable crystalline silica have been shown to cause silicosis. Silicosis is a disease that produces fibrous tissue in the lungs and is the result of the inhalation of freshly fractured crystalline silica.[46] The alveolar macrophages of the lungs ingest the deposited silica particles. Experimental observations have led to the concept that silica induces lung fibrosis by causing cell breakdown within the macrophage, macrophage death, and the release of collagens (insoluble proteins formed in the lungs that may eventually lead to lung scarring).[47] Silicosis is a chronic disease that may progress for decades before significant or detectable respiratory symptoms develop.[48]

During this investigation, analysts reviewed applicable medical databases, such as MEDLINE� and TOXLINE�, for information related to health effects from exposures to various chemicals and hazardous substances. MEDLINE�, the US National Library of Medicine's premier bibliographic database, contains over 11 million references to journal articles in life sciences with a concentration on biomedicine. TOXLINE�, the Library of Medicine’s extensive collection of bibliographic information, covers the biochemical, pharmacological, physiological, and toxicological effects of drugs and other chemicals. The results of the review indicated that, at the time of the initial release of this report in July 2000, there were no reports of silicosis from desert exposures among US military personnel. A review of the DoD Incident Reporting Line and Comprehensive Clinical Evaluation Program databases produced similar results.

However, there are references in the general literature to a "Desert Lung Syndrome." Korenyi-Both, et al. (1992) report on an acute desert-related disease they allege was caused by a mixture of fine sand and pigeon droppings.[49] Without data or pathology presented, the authors theorized that the sand triggered an extreme allergic reaction in a cohort of hospital personnel stationed at Al Eskan village near Riyadh, Saudi Arabia, from January to March 1991. They further postulated that in some cases, pathogens believed to originate in pigeon droppings might have further complicated the condition. The authors contend that in combination, this mixture contributed to an opportunistic lung infection in US military personnel so exposed. Again, there is no evidence to support this conclusion, nor is there any evidence of opportunistic lung infections in deployed servicemembers.

2.  Soot

Soot is a combination of particles impregnated with tar and formed by the incomplete combustion of a carbon-based material.[50] Health effects studies on soot are generally absent in the literature because of its amorphous nature and because it is often considered a component of PM. To compensate, the HRA uses carbon black as a surrogate for soot because human health effects data and established occupational exposure standards are available for carbon black, and because the USAEHA data from the Gulf War shows the soot to be a well-combusted, carbon-based material similar in properties to commercial carbon black.[51]Exposure to carbon black results in health effects that are dissimilar to those caused by exposure to silica. For example, respirable carbon black does not promote pulmonary fibrosis, as does silica. When inhaled by laboratory animals it produces little or none of the collagen produced fibroids seen in individuals suffering from silicosis.[52] Health effects from carbon black include reduced pulmonary function and irritation of the respiratory tract. These symptoms occur at concentrations of carbon black above 3.5 mg/m3, the Occupational Safety and Health Administration (OSHA) permissible exposure limit.[53] This standard is based on an exposure of 8 hrs per day, 365 days per year over a working lifetime of 30 years. (There is no authority to implement or enforce US standards in countries where US forces are deployed. US standards are cited for comparison or as reference points.)

| First Page | Prev Page | Next Page |