For Further Information write or call:

Division of Laboratory Sciences (F-20)
National Center for Environmental Health
Centers for Disease Control and Prevention (CDC)
4770 Buford Highway, N.E.
Atlanta, GA 30341-3724

Telephone: (770) 488-4151
Fax: (770) 488-7075

July 24, 1987 / 36(28);470-5

Serum Dioxin* in Vietnam-Era Veterans -- Preliminary Report

Agent Orange, a defoliant used in Vietnam, was a mixture of 2,4-DD and 2,4,5-TS. During manufacture 2,4,5-T was contaminated with TCDD*, a compound with marked toxicity in some species of experimental animals (1-4). In 1979, the U.S. Congress responded to concerns of Vietnam veterans by passing Public Law 96-151 mandating epidemiologic studies of the possible health effects on Vietnam veterans of exposure to herbicides and their associated dioxin contaminants. In 1983, CDC developed a protocol (5) for a historical cohort study (the Agent Orange Exposure Study) of U.S. Army veterans who had served in heavily sprayed areas of Vietnam. The protocol specified that the degree of exposure to Agent Orange be based on a score estimating the "likelihood of exposure" and calculated from information in military records.

Men who served in the III Corps military region (around Saigon) during the period 1967-1968 were selected for study because this region was heavily sprayed during that time. The U.S. Army and Joint Services Environmental Support Group (ESG) found that 65 U.S. Army combat battalions had spent at least 18 months in the III Corps area during the period 1967-1968. The ESG abstracted daily locations of companies within these battalions from military records and obtained personnel records of men who had served in those companies. Using existing records of each application of Agent Orange by fixed-wing aircraft, helicopter, or ground-based equipment and ESG troop location data, CDC developed several different methods for computing exposure scores for each man. These methods were based on each man's daily proximity (in time and space) to recorded Agent Orange applications.

Subsequent evaluation of military records by CDC and ESG revealed that daily tracking of individual soldiers was not always possible. The ESG evaluation also suggested that many helicopter and ground-based sprays, which were often near troops, were not recorded. Consequently, CDC has conducted a validation study using current TCDD levels in serum as a biological marker to determine whether scores based on military records or on veterans' self-assessed exposures to herbicides could identify those veterans who had received heavy exposure in Vietnam.

During 1986, CDC's Division of Environmental Health Laboratory Sciences, Center for Environmental Health, developed a method for measuring TCDD in human serum. The measurement, which is based on lipid weight, is highly correlated with paired measurements of TCDD in adipose tissue (r=.98) (6,7). The same laboratory subsequently used paired sera (drawn in 1982 and 1987) to estimate the half-life of the TCDD body-burden in man as approximately 6-10 years (CDC, unpublished data). The sera came from Air Force personnel involved in spraying Agent Orange in Vietnam during 1968. Some of these sera still show markedly elevated TCDD levels in 1987. These new developments suggest that only about 2 to 2.5 TCDD half-lives have elapsed since potential exposure in Vietnam and that serum TCDD can serve as a biological marker for previous Agent Orange exposure. These findings are the basis for the study of U.S. Army veterans reported here.

Vietnam veterans invited to participate in this study had served in at least one of the 65 selected battalions between October 1966 and March 1969. They were chosen from the 9,727 men whose records were sufficiently complete for exposure scoring and who met the original selection criteria proposed in 1983 (e.g., only a single tour of duty in Vietnam and pay grade of E1 to E5 at discharge). The exposure score used to select Vietnam veteran participants was the total number of occasions on which the veteran's unit was within 2 km of a documented Agent Orange spray within 6 days after that spray. This score is based on the assumption that TCDD undergoes rapid degradation on vegetation (8-10). All but 10))P of the 314 men with a high exposure (a score of 5 or more) were invited to participate in this study. A stratified random sample of 235 of the 1,351 men with a score from 1 to 4 were invited, and a sample of 440 of the remaining 8,062, all of whom had a score of 0, were invited. These men averaged over 300 days of service in Vietnam. A stratified random sample of 200 non-Vietnam veterans of the same era were invited as a comparison group. While they did not have Vietnam-related exposure to Agent Orange, their demographic and other personal characteristics were similar to the Vietnam veterans. Of the 979 invited Vietnam veterans, 871 (89) completed telephone interviews, and 665 (68) also completed medical examinations and gave blood for TCDD measurement at CDC. Those reporting health problems in the telephone interview were more likely to participate in the examinations and blood sampling than were those reporting good health. Of the 200 non-Vietnam veterans invited, 103 (52) participated fully. This lower participation rate does not affect exposure scores or TCDD levels in Vietnam veterans. Each participant underwent a detailed interview regarding military and civilian exposures to herbicides. Table 1 shows selected characteristics of the participants by exposure groups. While 25 of Vietnam veterans reported direct exposures (present during spraying or handled spraying equipment) and 70 reported indirect exposure (walked through defoliated areas), 6 of non-Vietnam veterans reported such exposures. Those who were both interviewed and examined were similar with respect to the characteristics shown in Table 1 to those who were interviewed only.

The preliminary TCDD distributions, which are shown in Figure 1 and are based on the first 519 specimens processed, represent a 68 random sample of the participants. All of these men except one had TCDD levels (based on lipid weight) below 20 parts per trillion (ppt), which is considered the upper limit for residents of the United States without known TCDD exposure (6,7,11,12). There was no significant difference among the three Vietnam veteran exposure groups selected on the assumption of short environmental availability of TCDD (p=.83). Likewise, no association was found between TCDD levels and two other methods of scoring exposure that were chosen to reflect a longer environmental persistence of TCDD (one method accounted for the distance from the spray, without regard to the time since spraying, and the other accounted for total days spent in heavily sprayed areas). Finally, no association was found between TCDD levels and self-perceived herbicide exposure in the military (either direct exposure or delayed exposure). The median TCDD levels for all exposure groups were between 3.5 and 4.3 ppt. Furthermore, TCDD medians for Vietnam veterans (median = 3.8 ppt) and non-Vietnam veterans (median = 3.9 ppt) were virtually the same. A full report will be published after TCDD measurements have been completed for all participants and the full report has been reviewed by the Agent Orange Working Group of the Domestic Policy Council (Executive Branch) and by the Congressional Office of Technology Assessment. Reported by: Agent Orange Projects, Div of Chronic Disease Control, Div of Environmental Health Laboratory Sciences, Center for Environmental Health, CDC.

Editorial Note

Editorial Note: The purpose of this study was to determine whether estimates of exposure based on military records or on interviews of U.S. Army veterans can identify those with heavy exposure to TCDD. Serum TCDD levels measured in 1987 were not associated with any of the indirect exposure scoring methods evaluated. Because of the purpose of the study, men with higher exposure scores were deliberately over-sampled. The distribution of TCDD levels reported here cannot be generalized with confidence to all U.S. Army Vietnam veterans since the study did not use a random sample of all such veterans.

While CDC was processing sera from the U.S. Army veterans reported here, it was concurrently processing sera from other groups with known occupational exposure to dioxin prior to but not after 1970. Some of those who were occupationally exposed had TCDD levels more than 30-fold higher in 1987 (CDC, unpublished data) than the median levels of approximately 4 ppt reported here for Vietnam veterans.

The distribution of TCDD levels for the Vietnam veterans, with all but one below the upper limit for unexposed U.S. residents, suggests that few of the participants in this study have had unusually heavy dioxin exposure. No threshold level has been determined as yet for the health effects of TCDD on humans.

 

References

 

  1. Allen JR, Barsotti DA, Van Miller JP, Abrahamson LJ, Lalich JJ. Morphological changes in monkeys consuming a diet containing low-levels of 2,3,7,8-tetrachlorodibenzo-p-dioxin. Food Cosmet Toxicol 1977;15:401-10. 2. Norback DH, Allen JR. Biological responses of the nonhuman

primate, chicken and rat to chlorinate dibenzo-p-dioxin ingestion. Environ Health Perspect 1973;5:233-40. 3. Schwetz BA, Norris JM, Sparschu GL, et al. Toxicity of chlorinated

dibenzo-p-dioxins. Environ Health Perspect 1973;5:87-99. 4. Zinkl JG, Vos JG, Moore JA, Gupta BN. Hematologic and clinical

chemistry effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin in laboratory animals. Environ Health Perspect 1973; 5:111-8. 5. CDC. Protocol for epidemiologic studies of the health of Vietnam

July 24, 1987 / 36(28);470-5

Serum Dioxin* in Vietnam-Era Veterans -- Preliminary Report

Agent Orange, a defoliant used in Vietnam, was a mixture of 2,4-DD and 2,4,5-TS. During manufacture 2,4,5-T was contaminated with TCDD*, a compound with marked toxicity in some species of experimental animals (1-4). In 1979, the U.S. Congress responded to concerns of Vietnam veterans by passing Public Law 96-151 mandating epidemiologic studies of the possible health effects on Vietnam veterans of exposure to herbicides and their associated dioxin contaminants. In 1983, CDC developed a protocol (5) for a historical cohort study (the Agent Orange Exposure Study) of U.S. Army veterans who had served in heavily sprayed areas of Vietnam. The protocol specified that the degree of exposure to Agent Orange be based on a score estimating the "likelihood of exposure" and calculated from information in military records.

Men who served in the III Corps military region (around Saigon) during the period 1967-1968 were selected for study because this region was heavily sprayed during that time. The U.S. Army and Joint Services Environmental Support Group (ESG) found that 65 U.S. Army combat battalions had spent at least 18 months in the III Corps area during the period 1967-1968. The ESG abstracted daily locations of companies within these battalions from military records and obtained personnel records of men who had served in those companies. Using existing records of each application of Agent Orange by fixed-wing aircraft, helicopter, or ground-based equipment and ESG troop location data, CDC developed several different methods for computing exposure scores for each man. These methods were based on each man's daily proximity (in time and space) to recorded Agent Orange applications.

Subsequent evaluation of military records by CDC and ESG revealed that daily tracking of individual soldiers was not always possible. The ESG evaluation also suggested that many helicopter and ground-based sprays, which were often near troops, were not recorded. Consequently, CDC has conducted a validation study using current TCDD levels in serum as a biological marker to determine whether scores based on military records or on veterans' self-assessed exposures to herbicides could identify those veterans who had received heavy exposure in Vietnam.

During 1986, CDC's Division of Environmental Health Laboratory Sciences, Center for Environmental Health, developed a method for measuring TCDD in human serum. The measurement, which is based on lipid weight, is highly correlated with paired measurements of TCDD in adipose tissue (r=.98) (6,7). The same laboratory subsequently used paired sera (drawn in 1982 and 1987) to estimate the half-life of the TCDD body-burden in man as approximately 6-10 years (CDC, unpublished data). The sera came from Air Force personnel involved in spraying Agent Orange in Vietnam during 1968. Some of these sera still show markedly elevated TCDD levels in 1987. These new developments suggest that only about 2 to 2.5 TCDD half-lives have elapsed since potential exposure in Vietnam and that serum TCDD can serve as a biological marker for previous Agent Orange exposure. These findings are the basis for the study of U.S. Army veterans reported here.

Vietnam veterans invited to participate in this study had served in at least one of the 65 selected battalions between October 1966 and March 1969. They were chosen from the 9,727 men whose records were sufficiently complete for exposure scoring and who met the original selection criteria proposed in 1983 (e.g., only a single tour of duty in Vietnam and pay grade of E1 to E5 at discharge). The exposure score used to select Vietnam veteran participants was the total number of occasions on which the veteran's unit was within 2 km of a documented Agent Orange spray within 6 days after that spray. This score is based on the assumption that TCDD undergoes rapid degradation on vegetation (8-10). All but 10))P of the 314 men with a high exposure (a score of 5 or more) were invited to participate in this study. A stratified random sample of 235 of the 1,351 men with a score from 1 to 4 were invited, and a sample of 440 of the remaining 8,062, all of whom had a score of 0, were invited. These men averaged over 300 days of service in Vietnam. A stratified random sample of 200 non-Vietnam veterans of the same era were invited as a comparison group. While they did not have Vietnam-related exposure to Agent Orange, their demographic and other personal characteristics were similar to the Vietnam veterans. Of the 979 invited Vietnam veterans, 871 (89) completed telephone interviews, and 665 (68) also completed medical examinations and gave blood for TCDD measurement at CDC. Those reporting health problems in the telephone interview were more likely to participate in the examinations and blood sampling than were those reporting good health. Of the 200 non-Vietnam veterans invited, 103 (52) participated fully. This lower participation rate does not affect exposure scores or TCDD levels in Vietnam veterans. Each participant underwent a detailed interview regarding military and civilian exposures to herbicides. Table 1 shows selected characteristics of the participants by exposure groups. While 25 of Vietnam veterans reported direct exposures (present during spraying or handled spraying equipment) and 70 reported indirect exposure (walked through defoliated areas), 6 of non-Vietnam veterans reported such exposures. Those who were both interviewed and examined were similar with respect to the characteristics shown in Table 1 to those who were interviewed only.

The preliminary TCDD distributions, which are shown in Figure 1 and are based on the first 519 specimens processed, represent a 68 random sample of the participants. All of these men except one had TCDD levels (based on lipid weight) below 20 parts per trillion (ppt), which is considered the upper limit for residents of the United States without known TCDD exposure (6,7,11,12). There was no significant difference among the three Vietnam veteran exposure groups selected on the assumption of short environmental availability of TCDD (p=.83). Likewise, no association was found between TCDD levels and two other methods of scoring exposure that were chosen to reflect a longer environmental persistence of TCDD (one method accounted for the distance from the spray, without regard to the time since spraying, and the other accounted for total days spent in heavily sprayed areas). Finally, no association was found between TCDD levels and self-perceived herbicide exposure in the military (either direct exposure or delayed exposure). The median TCDD levels for all exposure groups were between 3.5 and 4.3 ppt. Furthermore, TCDD medians for Vietnam veterans (median = 3.8 ppt) and non-Vietnam veterans (median = 3.9 ppt) were virtually the same. A full report will be published after TCDD measurements have been completed for all participants and the full report has been reviewed by the Agent Orange Working Group of the Domestic Policy Council (Executive Branch) and by the Congressional Office of Technology Assessment. Reported by: Agent Orange Projects, Div of Chronic Disease Control, Div of Environmental Health Laboratory Sciences, Center for Environmental Health, CDC.

Editorial Note

Editorial Note: The purpose of this study was to determine whether estimates of exposure based on military records or on interviews of U.S. Army veterans can identify those with heavy exposure to TCDD. Serum TCDD levels measured in 1987 were not associated with any of the indirect exposure scoring methods evaluated. Because of the purpose of the study, men with higher exposure scores were deliberately over-sampled. The distribution of TCDD levels reported here cannot be generalized with confidence to all U.S. Army Vietnam veterans since the study did not use a random sample of all such veterans.

While CDC was processing sera from the U.S. Army veterans reported here, it was concurrently processing sera from other groups with known occupational exposure to dioxin prior to but not after 1970. Some of those who were occupationally exposed had TCDD levels more than 30-fold higher in 1987 (CDC, unpublished data) than the median levels of approximately 4 ppt reported here for Vietnam veterans.

The distribution of TCDD levels for the Vietnam veterans, with all but one below the upper limit for unexposed U.S. residents, suggests that few of the participants in this study have had unusually heavy dioxin exposure. No threshold level has been determined as yet for the health effects of TCDD on humans.

 

References

 

  1. Allen JR, Barsotti DA, Van Miller JP, Abrahamson LJ, Lalich JJ. Morphological changes in monkeys consuming a diet containing low-levels of 2,3,7,8-tetrachlorodibenzo-p-dioxin. Food Cosmet Toxicol 1977;15:401-10. 2. Norback DH, Allen JR. Biological responses of the nonhuman

primate, chicken and rat to chlorinate dibenzo-p-dioxin ingestion. Environ Health Perspect 1973;5:233-40. 3. Schwetz BA, Norris JM, Sparschu GL, et al. Toxicity of chlorinated

dibenzo-p-dioxins. Environ Health Perspect 1973;5:87-99. 4. Zinkl JG, Vos JG, Moore JA, Gupta BN. Hematologic and clinical

chemistry effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin in laboratory animals. Environ Health Perspect 1973; 5:111-8. 5. CDC. Protocol for epidemiologic studies of the health of Vietnam

August 17, 1984 / 33(32);457-9

Epidemiologic Notes and Reports Vietnam Veterans' Risks for Fathering Babies with Birth Defects

Vietnam veterans' risks for fathering babies born with serious structural birth defects were assessed using a case-control study. Case-group babies--those with serious structural defects--were born during 1968 through 1980 and registered by CDC's Metropolitan Atlanta Congenital Defects Program (MACDP). This program registers babies born with structural defects to women who are residents of the five-county metropolitan Atlanta area. To be included in the registry, a baby's defects must have been diagnosed during the first year of life and recorded on a hospital chart by a physician. The use of MACDP as the source of cases precluded analysis of other reproductive outcomes in the fathers or functional deficits, such as mental retardation, in the babies.

Control-group babies--those born without defects--were chosen from among 323,421 babies who were born in the same metropolitan area to resident mothers during the same period. They were frequency-matched to the case-group babies by race, year of birth, and hospital of birth. A total of 7,133 case-group babies and 4,246 control-group babies were eligible for the study. The decision to include fewer control-group babies than case-group babies was based on a review of the anticipated statistical power of the study.

In all, 4,929 mothers of case-group babies and 3,029 mothers of control-group babies completed interviews; fewer fathers completed interviews--3,977 from the case group and 2,426 from the control group. The major reason for parents' not participating in the study was that they could not be located after extensive searching.

Information about paternal military service in Vietnam was obtained during 1982 and 1983 through telephone interviews with the parents of the case- and control-group babies. Vietnam veteran fathers were asked if they believed they had been exposed to herbicides, such as Agent Orange. In addition, a five-level "Exposure Opportunity Index" (EOI) was defined based on activities that may have provided an opportunity for exposure to Agent Orange. Vietnam veteran fathers were given subjective scores by the staff of the Army Agent Orange Task Force reflecting their presumed opportunities for exposure to Agent Orange; the EOI scores were assigned on the basis of times and places of service in Vietnam and occupational duties. Scores were assigned without knowledge of the case/control status of the fathers. Both parents were questioned about a wide variety of other potential risk factors for birth defects. In addition, Vietnam veteran fathers were asked whether they had contracted malaria in Vietnam and whether they had taken malaria chemoprophylaxis there.

Defects occurring among the case-group babies were divided into 96 diagnostic categories for data analysis. Most of the 96 categories were comprised of specific defects, such as anencephaly, ventricular septal defect, and Down syndrome. Some categories were formed by grouping specific types of defects; one comprised all types of defects combined (i.e., the complete case series).

For each of these 96 categories, four hypotheses were tested: (1) whether veterans, excluding Vietnam veterans, were at different risk than nonveterans for fathering babies with birth defects; (2) whether Vietnam veterans were at different risk for fathering babies with birth defects; (3) whether Vietnam veterans who were judged by the Army Agent Orange Task Force to have had greater opportunities for exposure to Agent Orange had different risks for fathering babies with defects; and (4) whether Vietnam veterans who said during the interview that they had been exposed to herbicides, such as Agent Orange, were at different risk. Testing the first hypothesis determined whether, for the tests of the remaining three hypotheses, Vietnam veterans' risks should be compared with those of other veterans or with those of other veterans and nonveterans combined. Testing the second hypothesis was the main focus of this study.

Fathers of 428 case-group babies were Vietnam veterans; fathers of 268 control-group babies were Vietnam veterans. Fathers of 4,387 case-group babies and fathers of 2,699 control-group babies were not Vietnam veterans.

The estimated relative risk of Vietnam veterans' fathering babies with defects when all types of defects are combined was 0.97 (95% confidence limits 0.83-1.14). With few exceptions, the estimated relative risks of Vietnam veterans' fathering babies with defects in the remaining 95 defect groups were similar. Similarly, there was little evidence of different risks for Vietnam veterans who had been assigned higher Agent Orange EOI scores or for Vietnam veterans who had stated during the interview that they believed they had been exposed.

It was determined that, for most defect groups, Vietnam veterans' risks were neither higher nor lower than those of other fathers. In any large study in which multiple statistical tests are done, some exceptions are expected. Some of this study's exceptions are noted below. The estimated risks for fathering babies with spina bifida (imperfectly formed spinal cord) were higher for Vietnam veteran fathers who received higher EOI scores. Vietnam veterans who had higher scores had higher estimated risks for fathering babies with cleft lip with or without cleft palate. Vietnam veterans who received higher scores had higher estimated risks for fathering babies with defects classified as "Other Neoplasms," which include teratomas, neuroblastomas, hamartomas, dermoid cysts, lipomas, central nervous system tumors, Wilms tumor, and miscellaneous benign tumors. Vietnam veterans, in general, had a lower risk for fathering babies with cardiovascular defects classified as "complex" defects (two or more cardiovascular defects). Vietnam veterans who stated they had contracted malaria while in Vietnam had a higher estimated risk for fathering babies born with hypospadias.

No associations between risks of defects and use of malaria chemoprophylaxis were found. Reported by Chronic Diseases Div, Center for Environmental Health, CDC.

Editorial Note

Editorial Note: The most important conclusion to be drawn from this study is that the data collected contain no evidence to indicate that Vietnam veterans have had a greater risk than other men for fathering babies with defects when all types of serious structural birth defects are combined. This study cannot prove that some factor associated with service in Vietnam was or was not associated with the occurrence of rare types of defects, defects in the babies of selected individuals, or defects in the babies of small groups of veterans. The conclusion, however, that Vietnam veterans in general have not fathered, at higher rates than other men, babies with defects when all types of birth defects are combined is based on relatively strong evidence.

All parents are at some risk of having a baby born with birth defects. Because this risk is always there, it is called a "background risk." All men, whether Vietnam veterans or not, who father babies, have the same background risk--about two or three chances out of 100 that their babies will have serious structural birth defects.

Assessing Vietnam veterans' risks associated with exposure to Agent Orange is difficult. The measures of exposure that can be obtained today are imperfect, at best. The ability of Vietnam veterans to give valid reports of exposure is unknown, and the records used for the assignment of EOI scores were made for military purposes, not for health studies. This limitation makes it particularly difficult to assess whether the few statistically significant associations found in this study between defects and greater opportunity for exposure to Agent Orange are likely to reflect true effects of exposure or whether they are merely chance occurrences.

Moreover, the estimated relative risks for the exceptions presented here are rather low. These exceptions could conceivably be due to unmeasured confounding factors and may not be biologically significant. The same reasoning can be applied to the statistically significant association of malaria and hypospadias and the statistically significant association observed for babies with complex cardiovascular defects being fathered by Vietnam veterans.

A summary report of this study has recently been published (1), and a more comprehensive report is available from CDC. Copies of these reports can be obtained from CDC's Chronic Diseases Division, Center for Environmental Health.

 

Reference

 

  1. Erickson JD, Mulinare J, McClain PW, et al. Vietnam veterans' risks for fathering babies with birth defects. JAMA 1984:252;903-12.

Division of Laboratory Science
National Center for Environmental Health (NCEH)
CENTERS FOR DISEASE CONTROL AND PREVENTION (CDC)

Exposure of Air Force Veterans to Agent Orange in Vietnam

Air Force spraying Agent Orange in VietnamHealth problem

Graph showing Ranch Hand dioxin exposure index not correlated with serum dioxin levelsLab response

Health impact

February 13, 1987 / 36(5);61-4

Current Trends Postservice Mortality Among Vietnam Veterans

The CDC has recently completed the first phase of the Vietnam Experience Study (VES), a comprehensive study of the health of Vietnam veterans. The VES is a historical cohort study in which the health of 9,324 Vietnam veterans is compared with that of 8,989 non-Vietnam veterans who served in Korea, Germany, or the United States during the Vietnam era. Eligibility for the study was limited to male U.S. Army veterans who first entered military service between 1965 and 1971, who served a single term of enlistment, and who were discharged alive in the enlisted pay grades E-1 through E-5. Participants were randomly selected from computerized lists of accession numbers taken from the military personnel files of Army veterans who were discharged during the relevant time period.

The VES has three components: an assessment of mortality; health interviews of living veterans; and a clinical, psychological, and laboratory evaluation of a random sample of those persons who completed the health interview. The mortality component is the portion of the VES that has recently been completed; a summary of this phase follows (1).

Several methods were used to determine the number of deaths occurring among Vietnam veterans after discharge from active duty and before January 1, 1984. The result was nearly complete ascertainment of the vital status for both cohorts. In addition to an analysis based on the cause of death as specified on each death certificate, a medical review panel independently assigned an underlying cause of death using information from supplemental sources. These sources included personal physicians as well as hospital records, autopsy reports, and coroner and law enforcement files. Causes of death were coded according to the Ninth Revision of the International Classification of Diseases (2).

The study indicated that veterans of service in Vietnam experienced a 17% higher rate of postservice mortality than veterans who served in Korea, Germany, or the United States. The most noteworthy pattern of overall mortality was the changing difference between Vietnam and non-Vietnam veterans over time. During the first 5 years after discharge, Vietnam veterans had a mortality rate 1.5 times higher than non-Vietnam veterans (Table 1). During the succeeding years, there was essentially no difference between the two groups. This pattern was generally consistent across most demographic and military subgroups of veterans. When the data were stratified by type of military unit and military occupational specialty, the relative risk of postdischarge mortality for those less likely to have been in combat was similar to the risk for those who were more likely to have been in combat.

External causes, which include both intentional and unintentional injuries, accounted for most of the increased mortality in the early postservice period. Fatal injuries from motor vehicle crashes (MVC) were approximately two times more likely among Vietnam veterans than non-Vietnam veterans during this time (Table 2). A more detailed examination of MVC deaths did not indicate any particular factor that could explain the overall excess among Vietnam veterans. Data on the involvement of alcohol (available for 62% of MVC deaths) indicated that drinking did not account for this excess. Furthermore, the increased death rate was evident regardless of the time of day of the crash or the number of vehicles involved. Suicide and homicide showed similar increases in the early follow-up period, with both rate ratios being at or below 1.0 thereafter (Table 2).

Mortality from unintentional poisonings was elevated among Vietnam veterans throughout the follow-up period, although the number of such deaths was small (rate ratio = 2.5, 95% confidence interval (CI) = 0.88-6.92). Most of these involved the use of illicit drugs. When all drug-related deaths identified by the medical review panel were analyzed together (Table 2), the rate ratio between Vietnam and non-Vietnam veterans appeared to increase with the number of years since discharge. Furthermore, this excess was found almost exclusively among draftees; those assigned to tactical military occupational specialties; and those serving in Vietnam during 1968 or 1969, the years of heaviest combat activity.

Circulatory system diseases were the only natural causes of death for which the mortality rate among Vietnam veterans differed from that among non-Vietnam veterans. As compared with non-Vietnam veterans, Vietnam veterans had a notable deficit in such deaths (RR = 0.5, 95% CI = 0.25-0.99).

For all causes of death except suicide, statistical adjustment for potential confounders such as age at discharge, race, military occupational specialty, and pay grade at discharge had little effect on the results. For suicide, adjustment increased the RR in the early postservice period from 1.7 to 2.5 (death certificate data). Reported by Agent Orange Projects, Div of Chronic Disease Control, Center for Environmental Health, CDC.

Editorial Note

Editorial Note: The intent of this study was to assess the effect of military service in Vietnam on subsequent mortality. The "Vietnam Experience" includes a wide variety of factors that could influence health. These include psychological stresses associated with war, infectious diseases prevalent in Vietnam, and exposure to the herbicide Agent Orange.

Previous studies of Vietnam veterans reveal a similar excess of mortality from external causes among Australian Vietnam veterans (3). Deaths from suicide, homicide, and unintentional poisoning occurred more frequently among Australian veterans who had served in Vietnam than among other Australian Vietnam-era veterans. Mortality associated with MVCs was not elevated overall, but data suggested an excess in the youngest age group.

Findings on mortality from external causes from four other proportional mortality studies of U.S. Vietnam veterans are not consistent with this CDC study (4-7). These four studies showed no significant increases in deaths from MVCs (5), suicide and homicide, or unintentional poisonings (4) among U.S. Vietnam veterans.

Whereas the CDC study revealed a continuing excess of drug-related deaths among U.S. Vietnam veterans, the only substance-related excess among Australian Vietnam veterans involved deaths from alcohol-related natural causes (1). These discordant findings may reflect differences in in-service use of drugs and alcohol. While the use of illicit drugs by American troops in Vietnam was reported to be heavy (8,9), drug use among Australian soldiers was reported to be uncommon. However, alcohol use was reported to be heavy among Australian soldiers (3).

The lower mortality from circulatory diseases among Vietnam veterans is unexpected and may be a by-product of the selection process for assignment to Vietnam, which may have included consideration of cardiovascular fitness established during basic or advanced training. An opposite result was found in the Australian study, where mortality due to circulatory diseases was 90% higher among Vietnam veterans than among non-Vietnam veterans (3). Various indexes of cardiovascular morbidity measured in the other components of the VES may help to further explain these mortality findings.

The CDC findings for external-cause mortality are similar to previous observations of postservice mortality in U.S. Army veterans serving in combat areas during World War II and the Korean War (10). In contrast, broader cross sections of World War II veterans, which included both men who had served in war zones and men who had not, did not show either a difference or a deficit in postdischarge traumatic deaths (10,11), as did non-Vietnam veterans in the CDC study. These findings suggest that the postservice excess of traumatic deaths among Vietnam veterans may not be unique to the Vietnam experience, but rather, may be a consequence of the unusual stresses endured while stationed in a combat zone. The pattern of drug-related deaths, however, may be more specifically linked to combat intensity rather than to the result of an across-the-board effect of the war experience.

The mortality assessment of Vietnam veterans presented here is an incomplete evaluation of the health experience of this group. Additional data on the present and past health status of living Vietnam veterans will be forthcoming from the health interview and laboratory and psychological evaluation components of the VES. Because this group of veterans has not yet reached the age at which chronic diseases have an important impact on mortality, continued monitoring of mortality among VES participants may provide additional insights.

 

References