For the general population, benzene standards are set by the EPA for drinking water at 5 ppb (1 ppb = 3.20 µg/m3), with the ultimate goal of 0 ppb in drinking water and in lakes and rivers. NIOSH's recommended occupational TWA is 100 ppb, OSHA's TWA is 1000 ppb, and ACGIH's TLV is 500 ppb.
Benzene is ubiquitous in air, both in rural and urban areas as well as indoors. Table 3.1 lists benzene concentrations in several U.S. locations and at the Al Ahmadi hospital.
|Locations||Mean Concentration Range||Comments||References|
|Urban, summer 1986||EPA, 1987|
|73 km NW of Denver, CO||0.02-0.85||Rural, spring-fall 1982||Roberts, 1985|
|Urban, summer 1986||EPA, 1987|
|Staten Island, NY||6.6
|Urban, spring 1984||Singh, 1985|
|Elizabeth & Bayonne, NJ||3.0 max.
|Urban, daytime, fall 1981||Wallace, 1985|
|Elizabeth & Bayonne, NJ||2.7 max.
|Urban, at night, fall 1981||Wallace, 1985|
|Urban, summer 1986||EPA, 1987|
|St. Louis, MO||11.1
|Urban, summer 1985||EPA, 1987|
|Stinson Beach, CA||0.38 ± 0.39||Remote coastal, 1984||Wester, 1986|
|Al Ahmadi Hospital||4.2 Maximum||USAEHA, 1994|
Daily median benzene air concentrations for the period 1975-1985 are listed in Table 3.2. The outdoor air values include data from 300 cities in 42 states and the indoor air from 30 sites in 16 states (Shah, 1988).
SOURCE: Shah, 1988.
aThese measurements were made prior to current restrictions on smoking in the workplace. Current levels are most likely lower.
Benzene Concentrations in Air at Different Sites
|Inside home w/ 0 smokers||2.2||Wallace, 1989a|
|Inside home w/ 1 or more smokers||3.3||Wallace, 1989a|
|Inside a smoke-filled bar||8.1-11.3||Brunnemann, 1989|
|Breath of smokers||4.7||Wallace, 1989b|
|Breath of nonsmokers||0.47- 0.63||Wallace, 1989b|
|Breath of smokers in urban area||6.8±3.0||Wester, 1986|
|Breath of nonsmokers in urban area||2.5 ± 0.8||Wester, 1986|
|Breath of smokers in remote area||2.1 ± 9.6||Wester, 1986|
|Breath of nonsmokers in remote area||1.8 ± 0.2||Wester, 1986|
|In vehicle on NJ Turnpike||5.0 ± 6.0||Lawryk, 1995|
|In vehicle in Lincoln Tunnel, NY-NJ||8.1 ± 8.3||Lawryk, 1995|
|Municipal landfill||32||Wood, 1987|
|Kin-Buc Landfill, Edison, NJ (Superfund site)||59.5||Bennett, 1987|
|Love Canal basement, Niagara Falls, NY||162.8||Pellizzari, 1982|
Personal exposures to benzene tend to exceed the outdoor air concentrations. Data from the Total Exposure Assessment Methodology (TEAM) study (Wallace, 1989a) give a mean personal exposure of about 4.7 ppb, compared to a mean outdoor concentration of only 1.9 ppb. The same study also measured the median level of benzene inside homes without smokers and with one or more smokers. The results are included in Table 3.3. It is interesting to note that the personal level is higher than the level inside the home. A plausible explanation is that the personal value also includes exposures at other locations where daily activities of the study volunteer take him or her, i.e., in transit, inside a car, at work, etc.
Benzene intake during daily activities can be estimated. A smoker who consumes approximately two packs per day will have an additional daily intake of about 1200 µg of benzene (Fishbein, 1992). Assuming an urban concentration range of 2.8-20 ppb and an air intake of 20m3 per day, then the average air intake of benzene is 180-1300 µg per day. For a moving automobile with an average benzene concentration of 40 µg/m3 and an exposure duration of one hour per day, the benzene intake would be approximately 40 µg per day (Wallace, 1989a). Estimates of exposure from self-filling a car with gasoline and from evaporative emissions seeping into a home from automobiles in attached garages have been set at 150 µg per day (Wallace, 1989a).
Human studies show that inhalation exposure to benzene in the 1,000-ppb range (1 ppm = 1,000 ppb) from several months to several years reduces the number of all major blood cell types--erythrocytes (red blood cells), platelets, and leukocytes (white blood cells)--that are produced in the bone marrow. The next stage of severity is aplastic anemia, when the bone marrow ceases to function. Aplastic anemia can progress to acute myelogenous leukemia. Several occupational studies of workers exposed to low levels of benzene (approximately 25,000 ppb for nine years (Fishbeck, 1978) and 2,000-35,000 ppb (Townsend, 1978)) indicate a slight decrease in red blood count (RBC) at the end of the exposure period, but normal values years later. Significant decreases in white- and red-cell counts were recorded for workers exposed to 75,000 ppb for 10 years; for later years at lower exposures (15,000-20,000 ppb) their blood counts increased to normal values (Kipen, 1989). More severe effects, such as preleukemia or acute leukemia, were observed in workers exposed to 210,000-650,000 ppb for 1-15 years (Aksoy, 1978). Painters exposed to 3,000-7,000 ppb of benzene and other VOCs for 1-21 years showed increased serum immunoglobin (IgM) values and decreased values of IgG and IgA (Lange, 1973).
Multiple animal studies support the above observations (Rozen, 1984, 1985). Animal studies indicate a decrease in functional immune responses reflected in decreased resistance to infectious agents at benzene concentrations > 30,000 ppb for five days with recovery on the seventh day (Rosenthal, 1985).
The genotoxicity of benzene has been studied extensively. Benzene and its metabolites seem to be genotoxic to humans, causing primarily chromosomal aberrations (Major, 1992; Yardley-Jones, 1990; Sasiadek, 1989).
Experimental data for animals and studies of humans indicate a link between a decrease in bone-marrow cellularity and the development of leukemia. Many cases of benzene-induced leukemia seem to have been preceded by aplastic anemia (Toft, 1982). Benzene is considered a human carcinogen by U.S. and international agencies; the EPA classifies it as a Class A variety. The EPA estimated a risk value of 2.7 x 10-2 for leukemia due to a total lifetime exposure of 1,000 ppb inhaled benzene for concentrations in air below 31 ppb (EPA, 1986).
The Clean Air Act Amendments of 1990 list toluene as a hazardous air pollutant. OSHA's TWA is 200 ppm (= 200,000 ppb = 750,000 µg/m3); NIOSH's TWA is 100 ppm (= 100,000 ppb = 375,000 µg/m3); and ACGIH's TLV is 50 ppm (50,000 ppb = 188,000 µg/m3).
Studies of humans and animals have demonstrated that toluene is readily absorbed via the lungs and the gastrointestinal tract; it accumulates in adipose tissues (EPA, 1984). Elimination of toluene is primarily (approximately 2/3) via urine as hippuric acid and is usually complete within 24 hours of exposure. Low and intermediate levels of exposure to toluene primarily affect the central nervous system as summarized in Table 3.4 (Benignus, 1981). Effects were reversible, even at high-exposure levels for long durations.
|100 ppma||4 days @ 6 hours per day||Headaches, dizziness, and eye irritation||Andersen, 1983|
|600 ppm||8 hours||All of the above plus euphoria, dilated pupils, convulsion and nausea||Benignus, 1981|
|200-800 ppm||chronic||All of the above plus fatigue, muscular weakness, confusion, and accommodation disturbances||Greenberg, 1997;
|10,000-30,000 ppm||Narcosis and death||Echeverria, 1989|
appm = 1,000 ppb.Epidemiological studies revealed no significant increased risk for cancer among workers, but toluene may produce liver and kidney damage at high levels of exposure (Benignus, 1981).
Very little is known of its human health hazards compared to benzene and toluene, particularly chronic effects. Current animal data about whether xylene causes cancer are inconclusive. Epidemiological studies on cancer risks associated with toluene and xylene have to control for the known effects of benzene impurities (McMichael, 1988). Low levels (100-300 ppm) of inhaled xylene can cause eye, nose, and throat irritation, delayed response to visual stimuli, and reduced memory (Fishbein, 1985). NIOSH's and OSHA's TWA as well as ACGIH's TLV for m,o,p-xylene is 100 ppm. Exposure of workers in China to a mixture of toluene and xylene indicates that the effects of the combined toxicities are additive (Chen, 1994).
Background levels of the PAH group in air in the United States are reported to be in the range of 20-1200 µg/m3 in rural areas and 150-19,300 µg/m3 in urban areas. Personal air concentrations of benzo(a)pyrene in Padua, Italy, were estimated in winter and summer; the means were 370 µg/m3 and 121 µg/m3 respectively (Minoia, 1997). Similar measurements were taken on the street and inside a city park in Copenhagen, Denmark; the results were 4400 µg/m3 and 1400 µg/m3 respectively (Nielsen, 1996). Background levels of PAHs in drinking water are in the range of 4-24 ng/L.
Humans are exposed to PAHs by choice of lifestyle and culture. For example, a study of commercial suntan oils based on mineral or vegetable oils that were analyzed for PAHs showed that all the samples contained benzo[a]pyrene together with other mutagenic, co-carcinogenic or noncarcinogenic PAHs, fluoranthene, benzo[k]fluoranthene, and anthracene. The total PAH content of the samples varied from 89-189 ng/g, while benzo[a]pyrene levels were in the 2-5 ng/g range. The results suggest that users of suntan oils may be exposed to low levels of potentially hazardous PAHs (Monarca, 1982).
In another study, the levels of 13 PAHs were determined in smoked fishery products from both modern smoking kilns with external smoke generation and from traditional smoking kilns. The average benzo(a)pyrene (BaP) concentration in all 35 samples from modern smoking kilns was 0.1 µg/kg (wet weight). The sum of other PAHs determined in the study (benz(a)anthracene, chrysene, benzo(b)fluoranthene, benzo(k)fluoranthene, benzo(a)pyrene, dibenz(a,h)an-thracene and indeno(1,2,3-c,d)pyrene) was about 4.5 µg/kg (wet weight). The BaP levels of the 27 smoked fish samples from traditional kilns ranged from 0.2-4.1 µg/kg, with a mean value of 1.2 µg BaP/kg. The average concentration of the sum of the carcinogenic compounds was 9.0 µg/kg (Karl, 1996). Another dietary study from Italy calculated that the total dietary PAH intake was 3 µg per day per person, and the total intake of carcinogenic PAHs was 1.4 µg per day per person--high compared to the calculated inhalation of 0.370 µg per day in the most-polluted cities (Lodovici, 1995).
Scant information is available on the human health effects of specific PAH compounds. The limited health-effects data available arises from animal studies, where a wide range of effects have been found but only from exposure to extremely high doses of benzo(a)pyrene by ingestion, dermal contact, or prolonged inhalation (Sharma, 1997). The PAHs in these studies include anthra-cene, benzo(a)pyrene, benzo(b)fluoranthene, benzo(k)fluoranthene, chrysene, dibenz(a,h)anthracene, and indeno(1,2,3-cd)pyrene. There is no conclusive evidence that similar effects could occur in humans. However, the U.S. Department of Health and Human Services has determined that PAHs may reasonably be considered carcinogens.
Recent epidemiological studies report direct evidence of the carcinogenic effects of PAHs in occupationally exposed subjects. Risks of lung and bladder cancer were dose-dependent when PAHs were measured quantitatively against unexposed control groups. These findings suggest that the current threshold limit value of 200 µg/m3 of benzene-soluble matter, which indicates PAH exposure, may be too high; after 40 years of exposure, it gives a relative risk of 1.2-1.4 for lung cancer and 2.2 for bladder cancer (Mastrangelo, 1996). Studies indicate that when binary mixtures of some PAHs are administered, the yield of nuclear anomalies in the mouse gastrointestinal tract is less than expected by simple addition and closer to that expected by averaging the activities of the two PAHs comprising the mixture (Reddy, 1991).
Epidemiological studies on the health effects of particulate matter suggest significant short- and long-term toxicity at current ambient levels in the United States. So far, these effects seem to be less influenced by particle composition, inorganic versus organic, and nominal size than by gravimetric estimates of exposure. This appears to contradict the premises of conventional air-pollution toxicology, which is based on chemical-specific toxicity and the critical role of size in particle potency. The biological mechanism underlying the health effects found with PM10 in epidemiological studies is not well understood.
Time-series mortality studies suggest that an increase of 50 µg/m3 in the average 24-hour exposure to PM10 above the NAAQS is associated with an increased relative risk (RR) that ranges between 1.025 and 1.05 in the general population, and an even higher RR in at-risk subpopulations, i.e., the elderly and those with pre-existing respiratory conditions (Pope, 1996; Schwartz, 1996a, 1996b). The range of PM10-mortality RR across studies may reflect the likely differences in PM10 composition as well as differences in PM10-averaging periods considered in the analyses. Recent analyses of the Harvard Six City Study that was conducted in six eastern U.S. cities found larger associations between excess mortality and fine particles (PM2.5), than with coarse particles (PM10-PM2.5) alone (Schwartz et al., 1996). Moreover, the correlation of excess mortality with coarse-mass particles becomes not significant, except in Steubenville, OH, where the coarse particles are probably predominantly from industrial combustion sources (RR = 1.053 per 25 µg/m3 in PM2.5).
Many studies have investigated the relationship between hospital admissions, outpatient visits, and emergency room visits for respiratory and heart diseases and PM10 in conjunction with other pollutants, e.g., O3, SO2, CO, NO2, H+. These studies have used data from many cities in the United States and Canada (Burnett, 1994; Schwartz, 1994a,b,c, 1995a, 1996a; Gordian, 1996). Chronic obstructive pulmonary disease (COPD), pneumonia, and nonspecific respiratory-disease hospitalizations show moderate but statistically significant RR in the range of 1.06-1.25 when there is an increase of 50 µg/m3 in PM10 or its equivalent. Although a substantial number of hospitalizations for respiratory-related illness occur in those older than 65, there are numerous hospitalizations for those under 65 as well.
Many of these studies also examine the effect of O3, and collectively they indicate that ambient O3 has a significant effect on hospital admission for respiratory causes, with RR ranging from 1.1 to 1.36 per 100 ppb. For a two-pollutant model (PM10 + O3), the RR range is 1.04 to 1.54 per 100 µg/m3, while individually the RR for O3 is slightly lower than for PM10 (Schwartz, 1995a). The PM10 and O3 effects appear to be independent of each other, with no reduction in the RR for one pollutant after control for the other. Also, there is a suggestion of an effect between PM10 and heart disease; there is none for O3.
Studies of acute respiratory illness include upper respiratory, lower respiratory, or cough in children and in adults. Studies of upper-respiratory illness do not show consistent results. Three studies show a RR of 1.2 (Pope, 1991, 1992; Hoek, 1993), and another study estimates it as 1.55 (Braun-Fahrländer, 1992). These inconsistencies could be attributed to the difference in populations.
Studies of lower-respiratory disease give RR ranging from 1.10 to 1.28 (Pope, 1991, 1992; Hoek, 1993; Schwartz, 1991a) and another study set it at 2.0 (Schwartz, 1994). Studies of cough were more consistent, with RR ranging from 0.98 to 1.51 (Pope, 1992; Hoek, 1993; Schwartz, 1994; Dusseldorp, 1994). These estimated RR have a larger scatter than the corresponding RR derived from the hospitalization data. This variability is probably due to the former studies' populations including several different subgroups, whereas the hospitalization studies tended to include more uniform populations.
Limited evidence suggests pulmonary function decrements are associated with chronic exposure to particulate matter indexed by various measures--Total Suspended Particulate (TSP), PM10, sulfates, etc. (Spektor, 1991; Ackerman-Liebrich, 1997; Raizenne, 1996). These cross-sectional studies require a very large sample size to detect differences because of the inherent person-to-person variability; therefore, lack of statistical significance cannot be construed as proof of null effect.
Although virtually no human studies exist on the health effects of ultrafine particles, some relevant issues have been examined. A recent study on the effect of ambient-particle size on lung function and symptoms in asthmatics suggests that the effects of the number of ultrafine particles (diameter < 0.1 µm) may be greater than those of the mass of fine particles (diameters of 0.1 to 2.5 µm) (Peters, 1997). An animal study that investigated the surface coating of ultrafine particles suggests that acute exposure to near-ambient concentrations of sulfuric acid under conditions that promote the formation of acid as a surface coating on respirable particles can induce an enhanced nonspecific airway hyperresponsiveness (Chen, 1992).
About 42 percent of the Donora population experienced deleterious effects from its three-day smog episode. Mild upper-respiratory tract symptoms were evenly distributed through all age groups and on average lasted for four days. More than half of those above 55 complained of dyspnea, the most common symptom. The observed health effects could have been produced by two or more contaminants, i.e., SO2 and its transformation products in combination with other PM components (Schrenk, 1949; Hemeon, 1955).
The London smog episode of 1952 resulted in an estimated 4000 excess deaths. Hospital admissions increased dramatically, mainly among the elderly and those with preexisting cardiac or respiratory disease. Otherwise healthy pedestrians, their vision limited to as little as three feet, covered their noses and mouths in an attempt to minimize their exposure to "choking air" (United Kingdom Ministry of Health, 1954). As a consequence of the 1952 London episode, daily measurements of British Smoke (BS), related to PM and SO2, started in 1954. These historical pollution data indicate that extremely elevated daily acidic aerosol concentrations (approximately 400 µg/m3) may be associated with excess human mortality when present as copollutants with elevated concentrations of PM and SO2. At non-episode pollution levels (H2SO4 < 30 µg/m3), associations between acidic aerosols and mortality in London are statistically significant even though these associations cannot be separated from BS or SO2. Increased hospital admissions for respiratory causes were also reported (Ito, 1993). Studies in the northeastern United States and Canada, where high levels of acidic aerosols are present during the summer, indicate that the increase in respiratory hospital admissions associated with acidic PM10 is about six times that for nonacidic PM10 (Thurston, 1994).
Short-term exposures to sulfuric acid (H2SO4) aerosols (0.5 µm in diameter) at ambient levels can alter mucociliary clearance, the primary lung defense mechanism. In healthy and asthmatic adults, mucociliary clearance is initially increased at 100 µg/m3 of H2SO4 and then decreased for higher concentrations (300-1,000 µg/m3 ) (Leikauf, 1984; Spektor, 1985). Pulmonary function was also decreased in adult asthmatics at those exposures (Spektor, 1985). Animal studies support these findings and also show altered resistance to bacterial infection and altered alveolar macrophage function. Low-level H2SO4 (100 µg/m3) reacts synergistically with O3 by exacerbating the O3 lung-function effects. In these controlled laboratory studies, the H2SO4 exposures have been controlled nasal exposures (normal daily human exposure is also by mouth) where a significant acid neutralization by ammonia (NH3) may occur, thus reducing the deposited lung dose (Schlesinger, 1992a, 1992b).
|Elements||Urban||Rural||Remote||Camp Thunderock (August 1991)|
NOTE: Table 3.5 was updated November 21, 2005, to correct an error in the original table for the element Lead. In the original table, the concentration for Urban and Remote were transposed: the concentration for Urban was incorrectly shown in the Remote column and the number for Urban was in the Remote column. The numbers shown in red are the correct numbers. We have maintained the original Table 3.5 for historical purposes.
SOURCE: USAEHA, 1994.
ang/m3 = 0.001 µg/m33.
bMean concentrations in the Gulf region were in the range of rural areas in the U.S. except for nickel, which was at the urban level.
On the other hand, no metabolic oxidation of Cr (III) has been observed. The Cr (VI) sequestering capacity of whole blood and the reducing capacity of red cells explain why this metal is not a systemic toxicant except at very high doses. Reduction by fluids in the digestive tract, i.e., saliva and gastric juice, and sequestering by intestinal bacteria account for the poor intestinal absorption of Cr (VI). Chromium (VI) escaping reduction will be detoxified in the blood and liver. These processes explain the poor toxicity of Cr (VI) and its lack of carcinogenicity when introduced orally or swallowed following reflux from the respiratory tract. The chemical environment in the gastrointestinal tract and the blood is effective even under fasting conditions in reducing Cr (VI) to one or more forms of Cr (III) (Kerger 1997). Inhaled Cr (VI) is reduced in the epithelial lining fluid and in the pulmonary alveolar macrophages. The lung parenchyma has reducing capacity with slightly higher specific activity than the bronchial tree. Therefore, even in the respiratory tract, the only consistent target of Cr (VI) carcinogenicity has barriers hampering its carcinogenicity. This protection could be overcome only by massive exposure through inhalation, as in work environments lacking proper industrial hygiene (De Flora, 1997).
Some nickel compounds have been found to be carcinogens. Nickel carbonyl is correlated to nasal and lung cancer. Nickel subsulfide may be the most potent nickel carcinogen, but exposures to this compound are limited to specific occupations (Norseth, 1980). Other clinical manifestations include acute pneumonitis from inhaled nickel carbonyl, chronic rhinitis and sinusitis from inhaled nickel aerosols, and dermatitis and other hypersensitivity reactions from dermal exposures to nickel alloys (Sunderman, 1977). Cutaneous nickel allergy (contact dermatitis) affects 15-20 percent of the female general population and 1 percent of the males (Savolainen, 1996).
Short-term O3 exposure in healthy humans induces changes in pulmonary function, decreased volumes and flows, increased airway responsiveness, and airway irritation such as cough or pain on deep inspiration. Asthmatics experience similar effects and increased wheezing (Linn, 1994; Koenig, 1987, 1988; Molfino, 1991; Kulle, 1984). Inflammatory responses have been observed after acute exposures to O3 at concentrations found in U.S. cities (Devlin, 1990, 1991, 1996; Koren, 1990, 1991). Recovery from acute exposure is usually complete within 24 hours of the end of exposure. There is evidence of a plateau in lung volume in response to prolonged O3 exposure. Also, available data indicate that exposure to O3 for months and years causes structural changes in several regions of the respiratory tract. Research to date indicates that the area most affected is the centriacinar region, where alveoli and conducting airways meet (Sherwin, 1991).
There are very few human studies on binary pollutant exposure. Ozone in combination with SO2, H2SO4, HNO3, NO2, or peroxyacetyl nitrate (PAN) causes an additive response on lung spirometry or symptoms (Dreshsler-Parks, 1989; Aris, 1991; Hazuka, 1994; Utell, 1994; Koenig, 1990, 1994). Animal studies of O3 and NO2 or H2SO4 show that effects can be additive, synergistic, or even antagonistic, depending on the endpoint studies (Gelzleichter, 1992; Warren, 1986; Schlesinger, 1992a, 1992b). The chronic effects of co-pollutant exposure are still not understood. There is evidence suggesting that people with preexisting limitations in pulmonary function and exercise activity, e.g., asthma, COPD, chronic bronchitis, and ischemic heart disease, are at risk from O3 exposure.
There is a baseline blood level of COHb of approximately 0.5 percent for healthy adults and 1-8 percent for smokers. The most sensitive members of the general population to CO exposure are those with ischemic heart disease. They will start experiencing reduced exercise duration due to increased chest pain (angina) at CO levels that will give them 3-6 percent COHb (Kleinman, 1989; Allred, 1991). Healthy individuals will experience a reduction in their maximal exercise performance at CO levels that, after one hour, give them COHb levels of 2-3 percent. At COHb blood levels greater than 5 percent, healthy individuals may have equivocal effects on visual perception, audition, motor and sensory performance, vigilance, and other measures of neurobehavioral performance. At higher blood COHb levels, 10 percent or more, neurological effects could occur, including headache, dizziness, weakness, nausea, and confusion. Unconsciousness and death can occur with continuous exposure to high CO levels in a workplace or in unventilated rooms with faulty unvented combustion appliances.
The carcinogen potency of air pollution resides usually in the particulate fraction. Polycyclic organic chemicals and semivolatiles are associated with the particulate fraction and could have a prolonged residence time at sensitive sites in the respiratory tract when inhaled. Genetic bioassays have demonstrated potent mutagenicity, and presumably carcinogenic potential, of various chemical fractions of ambient aerosols. Copollutants such as irritant gases that initiate inflammation may promote carcinogenic activity (Lewtas, 1993).
|VOC||Kuwait City Personnel
SOURCE: Etzell, 1994.
Although the results from the heavy-metal analysis were difficult to interpret, because of a lack of "normal" ranges for cats as well as ignorance about what is "normal" for the region, the results seem reasonable when compared to other animal species. Analyses for vanadium and nickel were within normal limits, suggesting that the smoke was not a serious health risk. The clearance mechanism of the ciliated region of the lung apparently was efficient at eliminating particulate matter from the smoke. None of the lesions associated with prolonged exposure to respiratory irritants, and consistent with chronic bronchitis, chronic obstructive pulmonary disease, pulmonary fibrosis, or emphysema, was observed (Moeller, 1994).
The respondents in Group II recalled their complaints in Kuwait and compared them to those following their return. They reported that the persistence of symptoms was higher in Kuwait than during the eight weeks following their return to Germany. The increase in complaints (percent in Kuwait minus percent in Germany) for occasional symptoms were: eye irritation (27 percent), burning eyes (25 percent), shortness of breath (17 percent), weakness or fatigue (15 percent), skin rashes (14 percent), and respiratory irritation (14 percent). Symptoms were related to reported proximity to the oil fires, and their incidence generally decreased after the soldiers left Kuwait (Petruccelli, 1997).
Another self-administered symptoms questionnaire was developed by the U.S. Navy, and was completed by 2668 servicemen during March 28-31, 1991. Females were excluded because of their very small number. The respondents were divided into three categories according to their proximity to the oil well fires and duration of exposure. Group I consisted of 892 Marines who had the longest exposure, about five weeks at the time of the survey, and were closest to the burning oil wells. Group II included 978 Marines who had a short exposure to the oil fires, and were then stationed in Saudi Arabia about 120 km south of the Kuwait border. Depending on wind conditions, smoke from the oil fires would still have been clearly visible. Group III consisted of 831 Marines who had no direct exposure to the oil fires, having been located in southern Kuwait about 200 km south of the nearest oil field, where only a distant haze was visible on the horizon.
Marines in Group I reported the highest rate of gastrointestinal episodes and respiratory symptoms, followed by Group II. Similar patterns were observed for burning and red eyes. Adjusting for flu vaccination, history of respiratory disease, and smoking status, Group I reported wheezing, coughing, runny nose, and sore throat significantly more frequently than Group III. Group II reported significantly fewer colds than Group III. Smokers reported more complaints than nonsmokers. No patterns were observed when prevalence of respiratory symptoms within groups were examined by job class. The prevalence of wheezing, coughing, and runny nose for each group decreased from Group I to Group II to Group III, the latter being away from the smoke and on the coast away from blowing sand and dust (DoD, 1993).
A study was undertaken to assess and monitor the effects of the oil well fires on a squadron of 125 British bomb-disposal engineers who remained in Kuwait for five months. All subjects completed a health questionnaire and had their respiratory function measured. From June to October 1991, measurements were taken every two weeks; the subjects repeated the questionnaire just before returning to Britain. When data were stratified according to either smoking history prior to deployment or by amount smoked during the tour, no significant differences in either lung-function indices or symptoms were detected when compared to predeployment values (Coombe and Drysdale, 1993).
|Diagnostic Categories (ICD-9-CM Code)||Primary Diagnosis:Malesc||Primary Diagnosis:Femalesd||Primary Diagnosis:Alle||Any Diagnosis:Alle|
|Psychological conditions (230-219)||18.3||19.1||18.4||36.0|
|Symptoms, signs, and ill-defined conditions (780-799)a||18.1||16.5||17.9||43.1|
|Musculoskeletal system disease (710-739)||18.6||15.9||18.3||47.2|
|Respiratory system diseases (460-519)||6.9||6.1||6.8||17.5|
|Digestive system diseases(520-579)||6.5||4.9||6.3||20.4|
|Skin and subcutaneous tissue diseases (680-709)||6.3||6.0||6.2||19.9|
|Nervous system diseases (320-389)||5.3||8.8||5.7||17.8|
aIncludes conditions categorized according to ICD-9-CM nomenclature of cases for which no diagnosis was classifiable elsewhere; no more specific diagnosis could be made; signs or symptoms proved to be transient; cases in which a precise diagnosis was not available.
bIncludes registered participants without complaint or sickness as well as those diagnosed as normal or healthy.
The order of these diagnoses was determined by usual clinical practice, basing the ranking on the most severe conditions relative to the patient's chief complaints. The most prevalent primary diagnostic categories, accounting for 67.7 percent of the participants, were psychological conditions (18.4 percent); musculoskeletal and connective tissue diseases (18.3 percent); symptoms, signs, and ill-defined conditions (17.9 percent); respiratory diseases (6.8 percent); and digestive system diseases (6.3 percent). Nearly 10 percent received a diagnosis of healthy. When both primary and secondary diagnoses were considered, similar patterns emerged. The most common categories were musculoskeletal diseases (47.2 percent); symptoms, signs, and ill-defined conditions (43.1 percent); psychological conditions (36.0 percent); digestive system diseases (20.4 percent); skin and subcutaneous diseases (19.9 percent); respiratory diseases (17.5 percent); and nervous system diseases (17.8 percent).
Up to seven diagnoses, including healthy, could be reported (one primary and up to six secondary). Among the participants, 19.9 percent had only 1 diagnosis, 18.7 percent had 2, the median was 3, the mean was 3.4, and 9.1 percent were given 7 diagnoses.
The Iowa Persian Gulf Study Group is performing a follow-up study that includes a complete medical evaluation of a small random sample of the original cohort to verify the sensitivity and specificity of the larger study. The medical evaluation includes pulmonary-function tests that will also aid in verifying the small difference in lung-disease prevalence between the two military groups (Iowa Persian Gulf Study Group, 1997).
One must look cautiously at these studies because none includes quantitative measures of exposure or effects; findings are based solely on self-reported survey questionnaires administered years after the war's end. Some survey studies conducted years later probably have large uncertainties due to different recall and other biases.
Several factors may have made Gulf War veterans more vulnerable to pollutants. A significant number of Gulf War veterans were smokers and cannot be considered as having no lung impairment. Smokers react differently than nonsmokers to inhaled pollutants, even at a low concentration of irritants. Also, a small percentage of the veterans may have had some underlying predisposition to pulmonary disease such as asthma that might be triggered after exposure to high levels of PM10.
The levels of PM10 were extremely high, not because of emissions from the oil fires, but from the desert sand. These high levels of PM10 may perhaps explain the preliminary findings of the Iowa Study regarding respiratory symptoms as well as some of the respiratory symptoms reported in the CCEP. Although there are personal communications indicating that there were increased respiratory complaints among the indigenous population during the oil fires, no evidence of health effects or epidemiological studies were found in the peer-reviewed literature.
Genotoxic: denotes a substance that may cause mutation or cancer by damaging DNA.
Relative Risk (RR) is the ratio of probabilities that a disease will occur among those exposed to a factor to that of those not exposed.
As part of the Superfund Program, the EPA developed reference dose values (RfCs) for many toxic agents that estimate a daily exposure level for the general population that is likely to be without appreciable risk during a specific period. These estimates have been used to calculate cancer and noncancer risks (EPA, 1992).