Particles of about 10 �m or less in aerodynamic equivalent diameter are capable of reaching the alveoli (air sacks in the lung),^[24] and those measuring between 0.5 and 1.0 microns aerodynamic diameter have the highest possibility, percentage-wise, of being deposited in the alveoli.^[25] The lower respiratory tract clearance mechanism is highly efficient and capable of completely eliminating all particles smaller than five microns 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, say, 1000 particles per cubic centimeter, the efficiency level of the lower respiratory tract clearance system declines somewhat, so that only 90 percent of the particles will likely be eliminated.^[26]

Overall, health risks posed by inhaled particles are influenced by the concentration of particulate matter in the air, the duration of exposure, the penetration and deposition of particles in the various regions of the respiratory tract, and the body’s biological responses to these deposited materials. The largest particles are deposited in the air passages of the nose and sinuses (i.e., upper respiratory tract), with somewhat smaller particles depositing in the large and medium bronchi (i.e., middle respiratory tract). Still smaller particles can reach the gas exchange region of the lung (i.e., lower respiratory tract). In general, the risks of adverse health effects from the deposition of typical ambient fine particles in the lower respiratory tract are markedly greater than those from depositions in the upper air passages of the nose and sinuses.

Numerous studies have appeared in the recent literature on particulate matter epidemiology and have demonstrated an association between ambient particulate matter exposures and various acute health outcomes. Such outcomes include, for example, hospital admissions, increased respiratory symptoms, and decreased lung functions.^[27] Findings also suggest that: 1) infants, children, and the elderly may represent subgroups at higher risk for ambient particulate matter exposure effects; 2) cardiovascular causes of death and hospitalization in older adults may be a component of particulate matter-attributable mortality; 3) particulate matter health effects have been reported to be associated with several different particulate matter size fractions; 4) health effects may occur at different time scales for exposure to PM₁₀.^[28]

Epidemiology findings in the literature indicate that risk of death and the risk of the onset of disease due to lower respiratory disease (e.g., pneumonia) is increased by ambient particulate matter exposures. This may be due to exacerbation, by particulate matter, of a previously existing respiratory disease. Exposure to high levels of particulate matter may also increase susceptibility to infectious disease by decreasing clearance, impairing macrophage function, or through other specific and nonspecific effects on the immune system. The epidemiologic findings also indicate that individuals with preexisting infectious respiratory disease (e.g., pneumonia) are at increased risk for particulate matter effects.^[29]

While the focus of this report is on the exposures that may have resulted in the long-term unexplained illnesses reported by some Gulf War veterans, short-term inhalation exposures are also examined as a means of explaining some of the acute symptoms experienced by Gulf War veterans during and shortly after the war.

Dermal (skin) exposures to sand and soot can produce short-term, reversible symptoms. Anecdotal information suggests that some personnel experienced rashes, skin irritation and scaling. As noted by Thomas et al (2000), particulates containing silica in particular are associated with specific types of dermatitis and skin inflammation.^[30]

The inhalation of ambient levels of particulate matter observed in the KTO could have resulted in several acute symptoms and could have aggravated asthmatic conditions in some personnel. A number of recent studies have been conducted that examine the health effects associated with acute or short-term exposures to particulate matter.^[31] Daily lung function and/or respiratory symptoms were associated with changes in ambient PM₁₀ concentrations. These studies examined different health effect end-points for two study groups: 1) those who suffered from asthma; and 2) those who did not. Results were presented for the following end-points: 1) upper respiratory symptoms, 2) lower respiratory symptoms, or 3) cough. In general, study results indicated the following reversible symptoms as a result of acute exposures: cough, runny nose, phlegm, wheezing, and shortness of breath. A number of particulate matter exposure studies using different study groups are summarized by EPA (1999).^[32] These studies related PM₁₀ concentrations to observed health effects.

Adverse health effects from acute exposures to PM₁₀ may be confounded by the presence of other pollutants making it difficult to estimate that portion of risk attributable solely to PM₁₀. However, analytical results of air quality samples taken in the KTO in 1991 do not indicate that other air contaminants were at levels of concern.^{[33, 34, 35]} Nevertheless, uncertainties persist with this type of analysis suggesting that this issue is a candidate for further research.

Chronic pulmonary function studies are less numerous than acute studies and the results are inconclusive and in some cases inconsistent in findings. Some studies show effects for some endpoints, but other studies fail to find for the same effects.^[36] The limited number of studies that have been completed have used children as the study group. None of the recent studies have focused on a study population similar in age, health, and physical ability to that of Gulf War veterans. Therefore some other means of estimating the chronic effects of exposure is necessary and will be discussed in the next section.

Since airborne particulate matter is not a single pollutant, but rather a varying mixture of pollutants each with its own subclass of different chemical species, it is difficult to estimate the total risk of adverse health effects from exposure to particulate matter based solely on the analysis of its individual component species. That is, the risks are not necessarily additive. However, a reasonable estimate of the chronic or long-term risks 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 (i.e., they are capable of inducing changes or damage to lung tissue and cells); and 3) were associated with or originated from a source that potentially represents a major health concern (e.g., oil well fire smoke). With these factors in mind, silica and soot have been identified as potential contaminants of concern as found in the particulate matter concentrations measured in air samples taken in the KTO in 1991. In an occupational environment (which typically involved a long-term exposure) both contaminants have been found to result in respiratory distress, often leading to chronic effects, and reduced pulmonary function. Because of the inconsistencies and uncertainties associated with the chronic health effects studies noted previously, an examination of these constituents may be useful to estimate the relationship between particulate matter exposure and potential chronic effects. In other words, could the short-term exposures experienced by US personnel to particulate matter 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.

Silica exposures and associated health effects have been studied extensively in an occupational environment. The deposition of silica containing dust in the lungs has been researched and reported among the inhabitants of the Saharan, Libyan, Negev and Arabian Deserts. After years of exposure, individuals in these populations tend to develop a benign, non-progressive pneumoconiosis (disease of the lung characterized by fibrosis). This condition, sometimes referred to as Desert Lung Syndrome, differs from occupational silicosis (as found in some industrial or mining settings) in that it is asymptomatic (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."^[37] Old sand dust particles have surfaces that have been weathered or transformed over time. New dusts are particles of more recent origin; that is, they are freshly fractured (i.e., broken, sharp, and exposing new surface area).

Freshly fractured silica (caused by crushing, grinding, blasting, etc.) 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.^[38] 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 particulate matter collected after the Gulf War did not differentiate between "old" and "new" dust. Although the Gulf War exposures probably involved "old" dust, Thomas et al, in determining risks associated with exposure to silica containing particulate matter, adopted a conservative approach that assumed all silica was "new" or freshly fractured.^[39]

In the workplace long-term or chronic-exposures to respirable crystalline silica, however, have been shown to cause silicosis. Silicosis is a disease that produces fibrous tissue in the lungs and is caused by the inhalation of freshly fractured crystalline silica.^{[40, 41]} The alveolar macrophages of the lungs ingest the deposited silica particles. 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).^[42] Silicosis is a chronic disease that may progress for decades before significant or detectable respiratory symptoms develop.

A review of the medical databases (e.g., MEDLINE, TOXLINE) indicates that there are 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.

There are, however, references in the general literature to the so-called "Desert Lung Syndrome." Korenyi-Both, et al. (1992) report on an acute desert-related disease caused by a mixture of fine sand and pigeon droppings.^[43] 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.

The Thomas report describes soot as a combination of particles impregnated with tar and formed by the incomplete combustion of a carbon based material.^[44] The Thomas report 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.^[45] 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.^[46] Health effects from carbon black include reduced pulmonary function and irritation of the respiratory tract. These symptoms occur at high concentrations of carbon black over extended periods of exposure.^[47]

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