9
ADDITIONAL HEALTH EFFECTS

This chapter reviews the evidence concerning long-term, nonmalignant health outcomes that persist after cessation of exposure to insecticides or solvents. The immediate health effects of exposure to those agents are described in Chapters 3 and 4. In this chapter, a number of health outcomes are discussed with background information presented before the descriptions of epidemiologic studies. The committee considers case studies and case series for the health outcomes described in this chapter, because some of these outcomes may be difficult to investigate epidemiologically due to their rare occurrence or lack of reporting mechanisms (such as disease registries). For some health outcomes discussed in this chapter, such as renal effects, there is a body of literature only on exposure to solvents.

APLASTIC ANEMIA

Aplastic anemia is a disorder of hematopoiesis that occurs when the bone-marrow stem cells fail to produce mature blood cells. Some patients with aplastic anemia progress into myelodysplastic syndromes. Although aplastic anemia can occur at any age, it is most common in young adults and the elderly. About 1000 new cases are diagnosed each year in the United States (Castro-Malaspina and O’Reilly, 1998). The disease is more prevalent in Asia than it is in Europe or North America. In a small percentage of cases, aplastic anemia is an inherited condition (such as Fanconi’s anemia). Risk factors for acquired aplastic anemia include exposure to certain drugs (such as chloramphenicol or sulfonamides), industrial chemicals (such as benzene), high doses of radiation, chemotherapy treatments, viral infections (such as Epstein-Barr virus), and immune diseases. However, for more than half the reported cases a cause cannot be determined.

Epidemiologic Studies of Aplastic Anemia and Exposure to Insecticides

Several studies have examined the risk factors for aplastic anemia in relation to exposure to insecticides and pesticides. In response to concerns about possible high rates of aplastic anemia in Thailand, a population-based, case-control study began in Bangkok in 1989 and was expanded in 1991 to include two rural regions of Thailand (Issaragrisil et al., 1996). Patients and control subjects were interviewed about medical and occupational histories, drug and pesticide use, and chemical and radiation exposures. Issaragrisil and colleagues (1997) examined grain farming and pesticide use in a study of 81 cases of aplastic anemia in Khonkaen, a rural region in Thailand. That study involved 295 control subjects selected from the same medical institutions where the cases had been identified. The researchers reported an increased risk associated with occupational pesticide exposure



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Gulf War and Health: Insecticides and Solvents, Volume 2 9 ADDITIONAL HEALTH EFFECTS This chapter reviews the evidence concerning long-term, nonmalignant health outcomes that persist after cessation of exposure to insecticides or solvents. The immediate health effects of exposure to those agents are described in Chapters 3 and 4. In this chapter, a number of health outcomes are discussed with background information presented before the descriptions of epidemiologic studies. The committee considers case studies and case series for the health outcomes described in this chapter, because some of these outcomes may be difficult to investigate epidemiologically due to their rare occurrence or lack of reporting mechanisms (such as disease registries). For some health outcomes discussed in this chapter, such as renal effects, there is a body of literature only on exposure to solvents. APLASTIC ANEMIA Aplastic anemia is a disorder of hematopoiesis that occurs when the bone-marrow stem cells fail to produce mature blood cells. Some patients with aplastic anemia progress into myelodysplastic syndromes. Although aplastic anemia can occur at any age, it is most common in young adults and the elderly. About 1000 new cases are diagnosed each year in the United States (Castro-Malaspina and O’Reilly, 1998). The disease is more prevalent in Asia than it is in Europe or North America. In a small percentage of cases, aplastic anemia is an inherited condition (such as Fanconi’s anemia). Risk factors for acquired aplastic anemia include exposure to certain drugs (such as chloramphenicol or sulfonamides), industrial chemicals (such as benzene), high doses of radiation, chemotherapy treatments, viral infections (such as Epstein-Barr virus), and immune diseases. However, for more than half the reported cases a cause cannot be determined. Epidemiologic Studies of Aplastic Anemia and Exposure to Insecticides Several studies have examined the risk factors for aplastic anemia in relation to exposure to insecticides and pesticides. In response to concerns about possible high rates of aplastic anemia in Thailand, a population-based, case-control study began in Bangkok in 1989 and was expanded in 1991 to include two rural regions of Thailand (Issaragrisil et al., 1996). Patients and control subjects were interviewed about medical and occupational histories, drug and pesticide use, and chemical and radiation exposures. Issaragrisil and colleagues (1997) examined grain farming and pesticide use in a study of 81 cases of aplastic anemia in Khonkaen, a rural region in Thailand. That study involved 295 control subjects selected from the same medical institutions where the cases had been identified. The researchers reported an increased risk associated with occupational pesticide exposure

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Gulf War and Health: Insecticides and Solvents, Volume 2 (relative risk [RR]=2.7, 95% confidence interval [CI]=1.1–6.6). For a subset (n=10) exposed to organophosphate insecticides, there was an elevated but equivocal increase in risk (RR=1.9, 95% CI=0.6–5.9). The authors state that selection bias is improbable as an explanation for the associations because of the low refusal rate, but they do not discuss the limitation of hospital-based case-control studies in selecting control patients or the possibility of recall basis. A companion study examined recent household insecticide use in the entire group of cases (n=253) and controls (n=1174) in Bangkok and in two rural regions of Thailand (Kaufman et al., 1997). Risk estimates were calculated for use of specific insecticides and for groups of insecticides, and multiple logistic regression analyses were used to control for confounding by concomitant use of more than one insecticide and for demographic variables. A moderate increase in risk was seen in the comparison of cases (n=32) and controls (n=117) that reported any exposure to an insecticide product that combined dichlorvos, propoxur, and cyfluthrin (a pyrethroid) (RR=1.7, 95% CI=1.1–2.8). However, for subsets of this exposure group, associations were increased but not statistically precise: regular use (RR=1.6, 95% CI=0.9–2.9) and application by the subject (RR=1.8, 95% CI =0.8–4.1). Evaluation of exposure to the classes of insecticides showed no trend with increasing exposure for the subsets that reported any exposure to carbamates (n=36) (RR=2.1, 95% CI=1.2–3.7), regular use of carbamates (n=19) (RR=2.0, 95% CI=1.0–4.1), or carbamates applied by the subject (n=11) (RR=2.3, 95% CI=0.8–6.5). No important increases were seen in the analyses that examined exposure to classes of insecticides (organophosphates, pyrethrins, or organochlorines). The authors acknowledge that the few positive associations could have occurred by chance in the course of conducting multiple comparisons. A case-control study of cases identified from the French national aplastic-anemia registry used interviews with 98 patients, 181 hospitalized control subjects, and 72 neighbor control subjects (Guiguet et al., 1995). Detailed information was collected about occupational history, including tasks, exposures, environmental conditions, and protection. Risk of aplastic anemia was not consistently elevated for occupational exposure to insecticides (n=18) compared with hospitalized controls (odds ratio [OR]=1.6, 95% CI=0.8–3.0) or with neighbors (OR=0.4, 95% CI=0.1–1.3). A case-control study in North Carolina evaluated the relationship between occupational pesticide exposure and fatal cases of aplastic anemia (Wang and Grufferman, 1981). Sixty deaths attributable to aplastic anemia were identified from state records; two controls that died in the same year were selected for each case. No relationship was found between deaths in cases with occupations that might have involved exposure to pesticides and the occurrence of aplastic anemia (RR=0.67, 95% CI=0.26–1.7). Unlike the studies from Thailand, subjects for this study were identified from death certificates rather than from a hospital-case registry, and occupations recorded on death certificates, rather than questionnaires, were used to evaluate potential exposure. The authors reported no relationship between trends in the use of organochlorine insecticides (including lindane) and the incidence of aplastic anemia. A number of studies have examined the relationship between hematologic parameters and exposure to insecticides. Those studies have the potential to provide evidence to support conclusions on aplastic anemia; however, because they generally examined workers with continuing exposures, they do not provide information about

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Gulf War and Health: Insecticides and Solvents, Volume 2 persistent or long-term effects. For example, Bhatnagar and colleagues (1980) studied workers at a pesticide-formulation factory in Agra, India. They compared blood samples from 42 employees who manufactured DDT, aldrin, lindane, malathion, parathion, and carbaryl with blood samples from 15 healthy subjects chosen as controls. The pesticide-exposed workers had lower hemoglobin (11 g/dL vs 14.48 g/dL). No attempt was made to control for dietary iron intake, age, sex, or other medical conditions that could have been confounding factors. It also could not be ascertained whether the observed changes were short- or long-term effects. The committee reviewed many other hematologic studies, but they did not provide information on persistent long-term health effects (e.g., Khan and Ali, 1993; Milby and Samuels, 1971; Morgan and Lin, 1978; Queiroz et al., 1999; Rosenberg et al., 1999; Straube et al., 1999; Traczyk and Rudowski, 1979; Vine et al., 2000). Summary and Conclusion A small number of case-control studies have examined exposure to insecticides in relation to aplastic anemia (Table 9.1). One study showed increased risk associated with exposure to a mixture of dichlorvos, propoxur, and a pyrethroid. Other studies have not shown substantially increased risks for insecticide exposure. The committee concludes, from its assessment of the epidemiologic literature, that there is inadequate/insufficient evidence to determine whether an association exists between exposure to the insecticides under review and aplastic anemia. TABLE 9.1 Selected Epidemiologic Studies: Aplastic Anemia and Exposure to Insecticides Reference Population Exposed Cases Estimated Relative Risk (95% CI) Case-control Studies Issaragrisil et al., 1997 Residents of rural Thailand   Organophosphate exposure 10 1.9 (0.6–5.9) Kaufman et al., 1997 Residents of Thailand     Dichlorvos, propoxur, cyfluthrin     Any exposure 32 1.7 (1.1–2.8)   Regular use 17 1.6 (0.9–2.9)   Applied by subject 8 1.8 (0.8–4.1)   Carbamates   Any exposure 36 2.1 (1.2–3.7)   Regular use 19 2.0 (1.0–4.1)   Applied by subject 11 2.3 (0.8–6.5) Wang and Grufferman, 1981 Residents of North Carolina in pesticide-exposed occupations 60 0.67 (0.26–1.7) Guiguet et al., 1995 Residents of France and insecticide exposure     Hospital control comparison 18 1.6 (0.8–3.0)   Neighbor control comparison 4 0.4 (0.1–1.3) Epidemiologic Studies of Aplastic Anemia and Exposure to Organic Solvents Most of the relevant research on aplastic anemia has focused on exposure to benzene; a few studies have examined other specific solvents or solvent mixtures.

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Gulf War and Health: Insecticides and Solvents, Volume 2 Benzene Exposure to benzene at high doses is hematotoxic and can result in destruction of bone-marrow precursor cells and, in turn, in a decrease in white-cell, red-cell, and platelet counts (Goldstein, 1988). The hematotoxicity and carcinogenicity of benzene have been extensively reviewed (e.g., ATSDR, 1997; IARC, 1987), and a brief overview of the toxicologic information is provided in Chapter 4. The metabolism of benzene, which occurs in the liver and to a lesser extent in the bone marrow, plays an important role in its toxicity. Benzene is metabolized to benzene oxide, an epoxide, through an oxidation reaction catalyzed primarily by cytochrome P450 2E1. Cytochrome P450 2E11/6 also participates in benzene biotransformation. Benzene oxide can then be metabolized to various compounds, including o-benzoquinone and p-benzoquinone, which are thought to be the two main metabolites that mediate the toxicity of benzene. Data from laboratory animals and humans show that benzene affects the bone marrow in a dose-dependent manner, causing anemia, leukopenia, and thrombocytopenia; continued exposure causes aplasia and pancytopenia1 (Bruckner and Warren, 2001). Benzene also has carcinogenic properties. In experimental animals, an increased incidence of malignant lymphomas and some solid tumors have been seen after exposure to high doses of benzene. As discussed in Chapter 6, benzene has also been associated with some types of leukemia in humans. Most of the human evidence associating benzene exposure with aplastic anemia comes from case studies (many published in the early to middle 1900s). Although exposure characterization methods were poor, it is estimated that benzene concentrations often exceeded 100 ppm2 (as summarized in Smith, 1996). The hypothesis of an association with benzene exposure raised by the case reports has been confirmed by several epidemiologic studies, although most of the population-based studies have focused on the relationship between exposure to benzene and hematopoietic cancers (see Chapter 6). As early as 1897, the deaths of four workers at a Swedish bicycle-tire factory were attributed to aplastic anemia associated with exposure to high concentrations of benzene (cited in Aksoy, 1985). A retrospective cohort study by Paci and colleagues (1989) examined exposures to potentially high concentrations of benzene among shoe-factory workers in Florence, Italy. During the period from 1953 to 1960, glues—estimated to be as much as 70% benzene by weight—were used in shoe manufacturing. When the researchers compared mortality rates for the 1950–1984 cohort of workers with national rates, they found increases for aplastic anemia in women (one case versus 0.2 expected) and in men (six cases versus 0.38 expected). The Italian national mortality rates combined all blood diseases, and the analysis resulted in standardized mortality ratios (SMRs) of 4.16 (95% CI not provided) for women and 15.66 (95% CI=5.47–32.64) for men. A retrospective cohort study examined hematopoietic malignancies and related disorders in a group of 74,828 workers in China who were employed in 1972–1987 in benzene-exposed departments of 672 factories (Dosemeci et al., 1994; Travis et al., 1994; Yin et al., 1996a,b). Mortality and morbidity data on this cohort were compared with data on 35,805 nonexposed workers employed during the same period. Physician investigators blinded to exposure information reviewed histopathologic information, pathology reports, 1   Pancytopenia is a nonfatal condition with below normal values of red cells, white cells, and platelets. 2   The allowable occupational-health standard for benzene has steadily decreased in the United States. In 1987, the permissible exposure limit (PEL) set by the Occupational Safety and Health Administration was reduced from 10 ppm to 1 ppm TWA (time-weighted average).

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Gulf War and Health: Insecticides and Solvents, Volume 2 and medical records of workers who developed hematologic neoplasms and related disorders. Yin and colleagues (1996a) reported nine cases of aplastic anemia in the benzene-exposed cohort as compared with no cases in the nonexposed population. Because the study used such a large population, it was possible to detect differences in relatively infrequent outcomes. Furthermore, there was a careful review of medical records to confirm the diagnoses. However, there is a possibility that the results were confounded by other occupational exposures. Potential risk factors for aplastic anemia were examined in a case-control study in Baltimore, Maryland. Linet and colleagues (1989) compared 59 cases of aplastic anemia diagnosed in 1975–1982 with 59 controls matched for age, sex, race, and geographic area and selected by random-digit dialing. An increased risk of aplastic anemia was associated with self-reported benzene exposure (OR=3.1, 95% CI=1.0–9.2). However, for the purposes of this review, the inferences from the study are limited by the fact that 41% of the patients with aplastic anemia were under 20 years old at diagnosis and would not have had substantial occupational exposures. Two other studies provide information on the relationship between benzene and aplastic anemia. In a case series from Turkey, Aksoy and colleagues (1984) reported that about 23% of patients with aplastic anemia had reported exposure to benzene. The study examined potential risk factors but did not have a comparison population. Ott and colleagues (1978) reviewed the deaths (1938–1970) of 594 workers chronically exposed to benzene at concentrations of 1 ppm to over 30 ppm at a Dow Chemical plant. One death from aplastic anemia was reported, whereas only 0.1 would have been expected. The relationship between changes in hematologic parameters and exposure to low concentrations of benzene has been extensively studied. However, the studies generally are cross-sectional and do not provide substantial information about persistent or long-term effects of interest in this review, and they generally have had inconsistent findings. When changes were seen in hematologic measures at low exposure, the differences (such as in hematocrit, hemoglobin, white-cell count and platelet count) often were not internally consistent with other measures (for example, an elevated mean red-cell volume would be expected but decreased mean corpuscular hemoglobin concentration would not). Changes in hematologic or immunologic parameters are not necessarily stages in the development of a pathologic process. For example, the finding of gradually lower numbers of blood cells does not mean that continued exposure would lead to the development of aplastic anemia. Examples of studies of hematologic parameters include the studies by Kipen and colleagues (Cody et al., 1993; Kipen et al., 1988, 1990) who followed a cohort of rubber workers exposed to varying concentrations of benzene. Studies of this cohort are described in Chapter 6 regarding cancer outcomes, particularly leukemia (Rinsky et al., 1981, 1987). During the period from 1940–1948, as benzene exposures gradually dropped from 137 ppm to 32 ppm, white-cell counts rose (from 6200 to 9591), red-cell counts rose (from 4.67 to 5.13), and hemoglobin rose (from 97.0 to 108.0) (Kipen et al., 1988). Those findings indicate that exposure to relatively high concentrations of benzene depressed the production of blood cells. In the years after 1948, when benzene exposure was much reduced, the values for white- and red-cell counts were within the normal ranges (although a nonexposed comparison group was not studied in the same period). A study by Collins and colleagues (1991) compared hematologic parameters of 200 workers at a chemical factory who were exposed to low concentrations of benzene (0.01–1.4

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Gulf War and Health: Insecticides and Solvents, Volume 2 ppm) with those of 268 nonexposed workers from the same factory. The study found no abnormalities in white-cell count, red-cell count, hemoglobin concentration, platelet count, or mean red-cell volume. The study did find that smoking affected many hematologic parameters, underlining the importance of controlling for confounding. Many other studies of the effects of benzene exposure on hematologic parameters that were reviewed provided no information on persistent long-term health effects (e.g., Aksoy et al., 1971; Bogadi-Sare et al., 1995, 1997; Collins et al., 1997; Khuder et al., 1999; Rothman et al., 1996; Tsai et al., 1983; Ward et al., 1996). Solvents Only a few studies have examined aplastic anemia in relation to exposure to other specific solvents or to solvents in general. Several of the insecticide-exposure studies described above also examined exposure to solvents. The population-based, case-control study in Thailand (Issaragrisil et al., 1996) compared 284 cases of aplastic anemia identified in 40 hospitals in Bangkok and 15 hospitals in rural areas. The study enrolled four hospital controls of similar age and sex for each case. Two hematologists confirmed the diagnoses of aplastic anemia. Using interviews with the case and control subjects, the researchers examined several risk factors for aplastic anemia. For the cases and controls drawn from Bangkok hospitals, there was a strong association with a history of solvent exposure (RR=4.6, 95% CI=2.5–8.7). About 40% of the total cases came from rural hospitals, and no association was noted when those cases were compared with their controls. The study reported positive associations for other risk factors (such as grain farming, hepatitis A, and low socioeconomic status) and multivariate analyses adjusted for the many possible confounders. However, the study presents little information on exposure-assessment methods, participation rates, or the conduct of the interviews. Also, such hospital-based case-control studies are vulnerable to selection and recall bias. Using the French national register of aplastic anemia, Guiguet and colleagues (1995) studied 98 patients with aplastic anemia (recorded in the register in 1985–1988) and two groups of controls: 181 selected from the same hospital as the cases and 72 referred by case patients from among neighbors. Interviews were conducted to determine occupational and medical histories, and a toxicologist coded the occupational exposures (any exposure or a “large level of exposure”). The study reported no association between aplastic anemia and exposure to all types of solvents compared with hospital controls (OR=0.9, 95% CI=0.5–1.7) or neighbor controls (OR=0.6, 95% CI=0.3–1.4). Analysis of exposure to various classes of solvents revealed no consistently increased risk; for example, for higher exposure to halogenated solvents, the OR was 1.3 (95% CI=0.6–2.7) compared with hospital controls. Although the study was limited by a 50% participation rate, interviews were conducted at diagnosis, and the investigators found no evidence of participation bias in the case group. The case-control study in Baltimore, Maryland, described above (Linet et al., 1989) found an association of aplastic anemia with self-reported exposure to paint (OR=6.1, 95% CI=1.2–29.7), but there was no association with the occupation of painter. The study reported a slightly elevated risk for aplastic anemia and exposure to any solvents (OR=1.1, 95% CI=0.5–2.7). However, as noted above, the inferences from this study are limited by the fact that 41% of the patients with aplastic anemia were under 20 years old at diagnosis and would not have experienced substantial occupational exposure.

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Gulf War and Health: Insecticides and Solvents, Volume 2 Although a number of studies of the effects of exposure to solvents, particularly ethylene glycol ethers, on hematologic parameters were reviewed, the studies did not provide information on the persistent, long-term health effects of concern in this report (e.g., Cardoso et al., 1999; Cook et al., 1982; Cullen et al., 1983, 1992; Kyvik et al., 1992; Shamy et al., 1994; Shih et al., 2000; Welch and Cullen, 1988). Summary and Conclusion The hematotoxicity of benzene’s metabolites has been well characterized in animal studies with strong evidence of a dose-response relationship. For more than a century, case studies have reported a direct association between chronic high-level exposure to benzene and aplastic anemia in humans. This association has been confirmed in studies of workers exposed to potentially high concentrations of benzene that found consistently increased risks of aplastic anemia (Table 9.2). The effects of low-level benzene exposure, however, have not been studied as fully, and there have been inconsistent findings regarding changes in hematologic parameters in studies of low level occupational exposure to benzene. Studies of exposure to solvent mixtures have not revealed consistent increased associations with aplastic anemia. Results are for cases with higher exposure as compared with hospital controls. The committee concludes, from its assessment of the epidemiologic and experimental literature, that there is sufficient evidence of a causal relationship between chronic exposure to benzene and aplastic anemia. There is inadequate/insufficient evidence to determine whether an association does or does not exist between exposure to other specific organic solvents under review or solvent mixtures and aplastic anemia. TABLE 9.2 Selected Epidemiologic Studies: Aplastic Anemia and Exposure to Organic Solvents Reference Population Exposed Cases Estimated Relative Risk (95% CI) Benzene Cohort Studies Paci et al., 1989 Shoe-manufacturing workers in Florence, Italy     Females 1 4.16a   Males 6 15.66 (5.47–32.64)a Yin et al., 1996 Workers in China 9 Indeterminateb Linet et al., 1989 Residents of Baltimore, Maryland 13 3.1 (1.0–9.2) Solvents Case-control Studies Issaragrisil et al., 1996 Residents of Thailand     Bangkok residents NA 4.6 (2.5–8.7) Guiguet et al., 1995 Residents of France     All types of solvents 27 0.9 (0.5–1.7)c   Halogenated solvents 16 1.3 (0.6–2.7)c   Hydrocarbon solvents 19 1.2 (0.6–2.3)c

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Gulf War and Health: Insecticides and Solvents, Volume 2 Reference Population Exposed Cases Estimated Relative Risk (95% CI) Linet et al., 1989 Residents of Baltimore, Maryland     Any solvents 12 1.1 (0.5–2.7) NOTE: NA=not available. aSMR was calculated for bloodborne diseases as a group. bStudy reported no nonexposed workers with aplastic anemia. CARDIOVASCULAR EFFECTS Cardiovascular disease is among the most common causes of death, chronic illness, and disability among adults in the United States. Most of the risk factors are related to lifestyle and family history, but occupational and environmental risk factors have been suggested for several cardiovascular outcomes. A potential for increased risk of ischemic heart disease is attributable to chronic exposure to carbon disulfide used in rayon manufacturing, and risk of cardiac arrhythmia is attributable to acute exposure to high concentrations of solvents (Fine, 1992; Kurppa et al., 1984). Exposure to some heavy metals, such as lead, also has been associated with the potential for intermediate cardiovascular outcomes, such as hypertension (Kristensen, 1989). Epidemiologic Studies of Cardiovascular Effects and Exposure to Insecticides The cardiac effects of the insecticides and insect repellents examined in this report have been discussed in the literature primarily in the context of acute poisoning (Roth et al., 1993; Saadeh et al., 1997). However, the insecticide literature is sparse regarding long-term cardiovascular health outcomes. Two studies examined hypertension in relation to exposure to insecticides and other pesticides. A study in Oregon reported no difference in average blood pressure between control subjects and workers who formulated phenoxy herbicides or other unspecified pesticides (Morton et al., 1975); it was limited by a lack of information about the degree of exposure among the participating workers. Sandifer and colleagues (1972) reported increased systolic blood pressure among pesticide formulators and pest-control operators but not among farmers, manufacturing workers, workers designated as peripherally exposed, and control subjects. Both studies examined workers currently exposed to pesticides, so it was not possible to separate long-term and short-term health effects. Evaluation of the long-term cardiovascular effects of exposure to insecticides was limited to data from mortality studies done primarily for purposes of assessing cancer risk. Many studies focused on pesticides in general and provided sparse exposure information. Most studies showed decreased cardiovascular mortality or no association but did not control for confounding by risk factors, such as smoking, family history of cardiac disease, and diet. The studies also were potentially limited by a selection bias known as the healthy-worker effect (see Chapter 2). For example, a study of 32,600 employees at a lawn-care service that used insecticides (including diazinon, carbaryl, and malathion), herbicides, and fungicides reported 17 deaths from arteriosclerotic heart disease (including congestive heart disease) (Zahm, 1997). Comparable US population mortality rates would project an expected 33.1 deaths (SMR=0.51, 95% CI=0.30–0.82). The cohort was generally young

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Gulf War and Health: Insecticides and Solvents, Volume 2 and had been employed for only a short period (mean=1.6 years). Pesatori and colleagues (1994) reported similar results for mortality in a cohort of 4411 structural pest-control workers in Florida. For deaths from arteriosclerotic heart disease, the SMR was 0.9 (95% CI =0.5–1.1). Summary and Conclusion Although a well-recognized complex of short-term, reversible cardiac effects is associated with some pesticide poisonings, there are few data on long-term cardiovascular outcomes. Data from cross-sectional studies of workers who have continuing exposure to insecticides do not offer insights into the long-term nature of the effects. Mortality studies of pesticide-exposed workers show no increased risk; however, the healthy-worker effect and other study limitations make it difficult to evaluate long-term outcomes. The committee concludes, from its assessment of the epidemiologic literature, that there is inadequate/insufficient evidence to determine whether an association exists between exposure to the insecticides under review and irreversible cardiovascular outcomes. Epidemiologic Studies of Cardiovascular Effects and Exposure to Organic Solvents The literature on cardiovascular effects of solvent exposure is primarily on the short-term consequences of acute exposure. For some solvents, short-term cardiovascular effects are known to occur following acute exposure (reviewed in Kristensen, 1989; Wilcosky and Simonsen, 1991). For example, a body of medical literature, primarily case reports, exists regarding the metabolism of methylene chloride to carbon monoxide and the later development of angina pectoris in susceptible persons as a result of increases in carboxyhemoglobin. Case reports also discuss cardiac sensitization and arrhythmia attendant on acute exposure to chlorofluorocarbons and, to a smaller degree, to chlorinated solvents. Since these effects are considered short-term and they occur soon after exposure, they would not be considered relevant for the time frame being considered for Gulf War veterans. The committee examined many cohort mortality studies that assessed excess mortality (usually with a focus on discerning elevations in cancer) among workers known to have been occupationally exposed to a variety of solvents. For the most part, the studies showed no effect or a decrease in cardiovascular diseases among the workers. Because of their study design, those studies do not control for the healthy-worker effect or for confounding attributable to cigarette smoking or other confounding factors. Due to the limitations in this type of study design for the purposes of this review, the studies are not reviewed in detail here. A meta-analysis by Chen and Seaton (1996) assessed 52 published mortality studies of occupational solvent exposure and calculated a pooled SMR of 0.87 (95% CI=0.86–0.88) for all circulatory disease. Although the committee did not include meta-analyses in the body of evidence it used for making a conclusion, that study provides an indication of the extent to which the healthy worker effect pervades the evidence related to cardiovascular outcomes. In a cross-sectional study, Kotseva and Popov (1998) examined cardiovascular effects attributable to occupational exposure to solvents (including benzene, xylene, and phenol) in a Bulgarian petrochemical factory. The study identified 345 workers and 345 age-

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Gulf War and Health: Insecticides and Solvents, Volume 2 and sex-matched control subjects and divided them into three categories: highest benzene, toluene, and gasoline exposures; high xylene and lower toluene, benzene, and gasoline exposures; and exposure primarily to phenol. Meaningfully higher prevalences of electrocardiographic abnormalities and higher mean systolic and diastolic blood pressure as compared to the controls were found among the exposed members of the first two groups, but not among those exposed primarily to phenol. Given the study design, the workers were being exposed to solvents occupationally at the time of the study and so were not considered exposure-free for the evaluation of persistent effects. A retrospective cohort mortality study of workers at a cellulose-fiber plant examined ischemic heart disease (IHD) in 1271 workers exposed to methylene chloride (Ott et al., 1983). The study did not report an increase in IHD mortality among workers compared with the general population, nor when the duration of exposure and followup interval for IHD were assessed. A study of male workers exposed to methylene chloride in the production of cellulose triacetate photographic-film base also did not find an increased risk of IHD (Hearne et al., 1990). Suadicani and colleagues (1995, 1997) reported on the Copenhagen Male Study, which began in 1970 as a prospective cardiovascular cohort study of 2974 men who were free of IHD at the study’s outset. At the time of the analysis, 184 men had had at least one IHD event; 258 members of the cohort reported occupational exposure to organic solvents. The adjusted RR comparing men exposed to solvents with unexposed men was 1.7 (95% CI =1.1–2.7). The occupational exposure assessment in this study was based on self-assessment of lifetime occupational exposure, which could lead to recall and misclassification bias. No information is provided about the timing of exposure and the development of myocardial infarction. Wilcosky and Tyroler (1983) examined mortality from heart disease among workers exposed to solvents in a rubber and tire manufacturing plant in Akron, Ohio. They identified 1282 white male, hourly-wage workers who were employed at the plant or had retired after at least 10 years of exposure. Exposure estimates were obtained from annual solvent-use charts prepared for major processing areas of the plant for 25 solvents. Each subject was identified as having been exposed to specific solvents through a review of which jobs he had held in the company and through a review of the list of solvents authorized for use in specific areas, according to the annual-use charts. Until 1967, the plant had authorized the use of carbon disulfide, known to be associated with atherosclerosis (and not among the solvents sent to the Gulf War). Most workers were exposed to more than one solvent, and several solvents were often used concurrently in the process areas. Several solvents showed associations with IHD mortality, but the associations were inconsistent when adjusted for age and other solvent exposures. The age-adjusted rate ratio for workers exposed to ethanol but not to carbon disulfide or phenol was 1.8; for workers exposed to phenol but not carbon disulfide or ethanol, it was also 1.8. The study did not control for confounding by other known cardiovascular risk factors, and misclassification of exposures probably occurred. The authors pointed out that “solvent authorization” did not necessarily guarantee solvent use. As a part of the Stockholm Heart Epidemiology Program, Gustavsson and colleagues (2001) identified 1335 persons surviving for at least 28 days after a first myocardial infarction. Control subjects were selected from a population registry and were sex-, age- and catchment-area-matched with the case subjects. Subjects were asked to complete

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Gulf War and Health: Insecticides and Solvents, Volume 2 questionnaires on lifetime occupational history, including descriptions and duration of work. An industrial hygienist assigned exposure levels on the basis of probability and intensity. Adjusting for age, sex, smoking, hypertension, weight, diabetes mellitus, and physical activity, the authors reported a RR estimate for organic solvent exposure of 1.26 (95% CI=1.02–1.55) for those with low exposure, 1.05 (95% CI=0.76–1.47) for medium exposure, and 1.49 (95% CI=0.94–2.35) for the highest category of exposure compared with the unexposed subjects. The analysis of exposure and duration showed no trend with increasing exposure (lowest exposure, RR=1.50, 95% CI=1.14–1.96; moderate exposure, RR=1.00, 95% CI=0.74–1.34; and highest exposure, RR=1.20, 95% CI=0.92–1.58). The authors performed additional analyses to account for latency periods and lag in the calculation of dose, but the models gave no closer fit to the data. Variations of exposure within similar jobs and errors in work-history information could have contributed to exposure misclassification. Summary and Conclusion Only a few studies on solvent exposure have examined long-term cardiovascular effects, and they show inconsistent results and no trend of increased risk with increasing estimated exposure. Cohort mortality studies have generally demonstrated decreases in cardiovascular disease, but do not account for the healthy-worker effect. Other occupational cohort and case-control studies are fraught with the difficulties of assigning subjects in a retrospective exposure assessment and of controlling for lifestyle and other risk factors. The committee concludes, from its assessment of the epidemiologic literature, that there is inadequate/insufficient evidence to determine whether an association exists between exposure to the specific organic solvents under review or solvent mixtures and irreversible cardiovascular outcomes. RESPIRATORY EFFECTS Many compounds that are used in industry or have been identified as environmental contaminants have been associated with the development of nonmalignant lung disease. Examples are chronic bronchitis and emphysema associated with cigarette smoking, asthma associated with toluene diisocyanate exposure, and pulmonary edema associated with exposure to chlorine gas. The major confounding factor in most occupational studies of respiratory outcomes is smoking. Exposure to dusts and various chemical compounds also must be considered. For example, although some agriculture-related respiratory diseases have a known etiology (such as silo filler’s disease, which results from inhalation of nitrogen dioxide in unventilated farm silos), it has not been possible to pinpoint the etiology of many respiratory effects from among the numerous agricultural exposures of concern, including dusts, fungi, pesticides, and fertilizers (do Pico, 1992). The literature on respiratory effects includes cross-sectional studies that examined lung function in relation to insecticide or solvent exposure. Often, the subjects were employed at the time lung function was assessed and so had ongoing exposures to the compounds of concern. Thus, it was often not possible to assess the persistence of changes in lung function after exposure had ended.

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Gulf War and Health: Insecticides and Solvents, Volume 2 Reference Population Exposed Cases Estimated Relative Risk (95% CI) Nietert et al., 1998 Systemic sclerosis patients in South Carolina, occupational exposure   Males   Solvents, maximal intensity 57 2.9 (1.2–7.1) Trichloroethylene, maximal intensity 10 3.3 (1.0–10.3) Females   Solvents, maximal intensity 4 0.6 (0.2–1.9) Trichloroethylene, maximal intensity 6 0.9 (0.3–2.3) Nietert et al., 1999 Systemic sclerosis patients in South Carolina, hobby exposure 178 1.1 (0.7–1.9) Bovenzi et al., 1995 Occupational exposures in scleroderma cases, Trento, Italy 4 9.28 (1.08–243.8) Rheumatoid arthritis Case-Control Studies Lundberg et al., 1994 Swedish registry cases of rheumatoid arthritis     Males     Substantial use of organic solvents 68 1.2 (1.0–1.6)   Spray painters and lacquer workers 6 2.4 (1.1–5.4)   Females     Substantial use of organic solvents 4 0.9 (0.3–2.8)   Launderers and dry-cleaning workers 7 1.5 (0.7–3.2) Undifferentiated connective-tissue disorder Case-Control Studies Lacey et al., 1999 Cases of undifferentiated connective-tissue disorder   Painting or paint manufacturing 5 2.87 (1.06–7.76) Paint thinners or removers 32 2.73 (1.80–4.16) Mineral spirits, naphtha, white spirits 18 1.81 (1.09–3.02) REFERENCES Abrams K, Hogan DJ, Maibach HI. 1991. Pesticide-related dermatoses in agricultural workers. Occupational Medicine 6(3):463–492. Adams RM. 1997. Occupational skin disorders. In: LaDou J, ed. Occupational and Environmental Medicine. New York: McGraw-Hill. Pp. 272–290. Akbar-Khanzadeh F, Rivas RD. 1996. Exposure to isocyanates and organic solvents, and pulmonary-function changes in workers in a polyurethane molding process. Journal of Occupational and Environmental Medicine 38(12):1205–1212. Aksoy M. 1985. Benzene as a leukemogenic and carcinogenic agent. American Journal of Industrial Medicine 8:9–20. Aksoy M, Dincol K, Akgun T, Erdem S, Dincol G. 1971. Haematological effects of chronic benzene poisoning in 217 workers. British Journal of Industrial Medicine 28(3):296–302. Aksoy M, Erdem S, Dincol G, Bakioglu I, Kutlar A. 1984. Aplastic anemia due to chemicals and drugs: A study of 108 patients. Sexually Transmitted Diseases 11(4 Suppl):347–350. Al-Shatti AK, El-Desouky M, Zaki R, Abu Al-Azem M, Al-Lagani M. 1997. Health care for pesticide applicators in a locust eradication campaign in Kuwait (1988–1989). Environmental Research 73(1–2):219–226. Alavanja MCR, Rush GA, Stewart P, Blair A. 1987. Proportionate mortality study of workers in the grain industry. Journal of the National Cancer Institute 78(2):247–252.

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