ARCHIVED - The Use of Herbicides at CFB Gagetown from 1952 to Present Day
Agent Orange Ex-gratia Payment
The new deadline for applications is June 30, 2011.
On December 22, 2010, the Honourable Jean-Pierre Blackburn, Minister of Veterans Affairs and Minister of State (Agriculture), announced that the Government of Canada is extending the one-time, tax-free ex gratia payment of $20,000 related to the testing of unregistered U.S. military herbicides, including Agent Orange, at Canadian Forces Base (CFB) Gagetown in 1966 and 1967.
For more information on eligibility criteria, contact Veterans Affairs Canada by visiting www.vac-acc.gc.ca or calling 1-866-522-2122.
For three days in June 1966 and four days in June 1967, Agent Orange, Agent Purple and other unregistered herbicides were tested at Canadian Forces Base (CFB) Gagetown in cooperation with the U.S. military to evaluate their effectiveness. These are the only known instances that these military test chemicals were used at CFB Gagetown. Agent Orange, Agent Purple and other unregistered herbicides are not used at the base today. The base uses only federally regulated herbicides for brush control during its annual vegetation management program.
In August 2005 the Department of National Defence, with participation from Veterans Affairs Canada, Health Canada, and additional departments and agencies, initiated a fact-finding mission to gain information on the history of herbicides tested and used at CFB Gagetown from 1952 to the present day, and the potential risks to human health and the environment. A major interdepartmental effort has occurred over the past two years to conduct the analysis necessary to provide all the facts.
An independent Fact-finding and Outreach Coordinator, Dr. Dennis Furlong, was named to oversee this process. His work included providing input on the plans and reports for each fact-finding task, as well as being the principal contact for those seeking information about herbicide testing and use at CFB Gagetown. The fact-finding tasks were conducted by contracted, highly qualified non-governmental experts.
The draft reports of the scientific research were peer-reviewed by qualified, independent experts. The contractors addressed their comments, and the final reports were provided directly and concurrently to the Ministers of National Defence, Veterans Affairs, and the Fact-finding and Outreach Coordinator. Reports involving human health aspects were also provided to the Minister of Health. The Fact-finding and Outreach Coordinator, accompanied by the appropriate experts, then shared the results of each report with the public.
All of the fact-finding tasks are now complete, and there is a much clearer understanding and greater knowledge of the testing and use of herbicides at CFB Gagetown. Scientific study from the excavations, soil, water and vegetation sampling, human health risk assessments, and the epidemiological study indicates that most people who lived near or worked at CFB Gagetown were not at risk for long-term health effects from the herbicides applied there. The science also indicates that the base is safe today.
Results of the Fact-finding Tasks
As part of the fact-finding initiative, the Department of National Defence committed to producing a comprehensive list of individuals and military units who were present at CFB Gagetown during the testing of Agent Orange, Agent Purple and other herbicides in 1966 and 1967, and during the eight to 12 weeks per year (between June and August) from 1952 to the present day when application of herbicides took place.
The contractor for this task, Canadian Development Consultants International Inc, compiled a database with relevant information on more than 115,000 individuals. Information that was not deemed to be of a personal nature (this includes such information as the names, ranks and units of some individuals, as well as the dates they were in Gagetown) was made public. Personal information (this includes such things as age, employee numbers, home addresses and family information) will not be made public.
Any information collected from individuals by the Fact-finding and Outreach Coordinator's office is also considered personal and will not be made public. Individuals who wish to submit a request for personal information may do so under the Privacy Act through the Directorate Access to Information and Privacy at National Defence.
The objective of this task was to review the history of the use of herbicides at the CFB Gagetown range and training area from 1952 to the present day, to compile a comprehensive database for this information, and to provide information on the types of herbicides used and how they were used.
The contractor, Jacques Whitford, determined that aside from the military products used in the herbicide trials in 1966 and 1967, the herbicides applied at CFB Gagetown over the past fifty years were regulated and commonly used across Canada. The herbicide application program at CFB Gagetown followed the policies, science, and best practices of the time, as regulated by Federal and Provincial governments. Where specific information could be obtained from historical records, rates of application of herbicides used at CFB Gagetown were either within, or in many instances lower than, the recommended application rates suggested by the manufacturer.
The purpose of this task was to conduct an environmental site assessment of the range and training area at CFB Gagetown.
Based on the laboratory tests, only concentrations of dioxins and arsenic in some of the soil samples exceeded the Canadian soil quality guidelines. The highest concentrations of dioxins in soil were found in the location of the 1967 test plots. Concentrations slightly above Canadian guidelines of dioxins in soil were also found in the Clones bivouac site, the Murphy bivouac site, the Enniskillen
Range, the 1966 test plots, and four other discrete sites in the range and training area. In a proactive precautionary measure, DND temporarily restricted site access to areas where dioxins concentrations were the highest (1967 test plots), as well as where human exposure to surface soils would be the most concentrated (in the bivouacs) until the results of a site specific risk assessment were completed. Further study determined that the dioxin levels in these areas posed no risk to human health.
Groundwater and surface water samples had concentrations of dioxins less than the Ontario Ministry of the Environment drinking water quality objective, which was used as a comparison due to the absence of a Canadian drinking quality guideline.
This task aimed to conduct a barrel investigation, and excavation program and analysis. During the excavation process, no herbicide barrels were discovered.
This task modelled how herbicides migrated through the air from aerial application in order to provide exposure scenarios for the health risk assessment identified in Task 3A-1.
The goal of this task was to assess whether herbicides and associated contaminants may have migrated through groundwater and/or surface water.
The contractor for this task, Jacques Whitford, concluded that it would be difficult, expensive and take considerable time to quantitatively estimate surface water migration. It is not possible to quantitatively estimate groundwater migration due to the variability of conditions across the base and the lack of adequate data on soils and geology. Cantox Environmental used the Jacques Whitford scoping report, together with a qualitative approach, to eliminate the water exposure pathway from further consideration in the health risk assessments.
The objective of this task was to conduct a historical human health risk assessment to determine how humans may have been exposed to herbicides and military test chemicals at the time of use, and the potential risks to human health. This study was done in three tiers. Tier 1 concentrated on the contaminants related to the 1966 and 1967 testing of unregistered military chemicals. Tiers 2 and 3 concentrated on all other years of registered herbicide use.
The contractor for this task, Cantox Environmental, concluded that the military chemicals tested at CFB Gagetown in 1966 and 1967, the known contaminants in the herbicides used at CFB Gagetown during the annual spray program in the period prior to the late 1960s, and the active ingredients in the herbicides used at CFB Gagetown during the annual spray program posed no long-term risk to human health and safety for most individuals. Those who were directly involved during applications or who worked in the bush immediately after application may have some increased risk. The contractor also concluded that the known contaminants in the herbicides used at CFB Gagetown during the annual spray program after the late 1960s posed no long-term risk to human health and safety.
For this task, a present day contaminated site human health risk assessment, using data gathered from Task 2B, was conducted to assess current exposures and human health risks for all contaminants of potential concern identified in the water, soil, sediment, and vegetation environmental media sampled and analyzed at CFB Gagetown.
The results of this task indicate there is currently no risk to human health (as a result of herbicide use) in the areas of the base where access was restricted as a precautionary measure following the environmental site assessment.
The objective of this task was to perform a literature review of all epidemiologic studies examining the relationship between herbicides (those applied at CFB Gagetown) and human health, and to conduct a descriptive epidemiological study to determine whether the communities surrounding CFB Gagetown had a higher incidence of illness as compared to the general population of the province of New Brunswick.
The contractor for Task 3B, Dalhousie University led by Dr. Judy Guernsey, concluded that the communities surrounding CFB Gagetown do not have a significantly higher incidence of illness, as compared to the province of New Brunswick.
A consolidated report for all parts of Task 3 was completed. This report includes the results of the epidemiology research integrated with the results of the human health risk assessments.
The purpose of Task 4 was to provide information on tissue dioxin concentrations in fish and freshwater clams sampled within the CFB Gagetown Range and Training Area. These data provide estimates to whether there is a potential risk to humans from consumption of fish and freshwater clams at CFB Gagetown.
The contractor for Task 4, G.A. Packman and Associates, concluded that the levels of dioxins in fish and freshwater clams at CFB Gagetown were either below or consistent with regulated limits and values for fish and freshwater clams from other locations.
DND Wide Herbicide Use Project
In 2006, Golder Associates Ltd. (Golder) was retained by Public Works and Government Services Canada on a series of contracts on behalf of the Department of National Defence (DND) to research, organise and analyse all available information concerning the herbicides used at each Canadian Forces (CF) site across Canada. An objective of this undertaking was to confirm whether tactical herbicides such as Agent Orange and Agent Purple tested in 1966 and 1967 at CFB Gagetown were ever tested at other current and former CF Bases, Stations or Wings.
Golder’s review of the information has found no evidence of spray applications of the tactical herbicides Agent Orange or Agent Purple at any Bases, Stations or Wings aside from CFB Gagetown. Records do indicate that the non-tactical and commercially available herbicides 2,4,5-T and 2,4-D were potentially concurrently used, stored or disposed at each of Carp (Ontario), CFB Chatham and CFB Gagetown (New Brunswick), CFB Borden (Ontario) and another unidentified site.
As such, evidence to-date is to the effect that Agent Orange and Agent Purple were only applied at CFB Gagetown.
Health Information Summary for CF Members
The following information was issued on behalf of the Canadian Forces Surgeon General. It was intended to assist CF medical staff in placing the health risk in context and to serve as a direct reference for concerned CF members who desire more detailed and specific information than is available from existing herbicide and dioxin information sheets produced by various health authorities.
This document summarizes the findings of scientific studies and reviews specific to Agent Orange or otherwise relevant to recent concerns regarding human exposure and health effects of unregistered herbicides tested at CFB Gagetown June 14-16, 1966, and June 21-24, 1967. This document is organized into four main sections. The first three sections ( "GENERAL INFORMATION" , "HEALTH EFFECTS" , and "FATE IN THE ENVIRONMENT" ) provide background information. Much of this background information is related to the United States use of Agent Orange and other herbicides during the Vietnam War and the scientific study of exposed U.S. Vietnam veterans. This background information is necessary to provide context for the discussion in section four ( "HEALTH EFFECTS FROM SPRAYING IN GAGETOWN" ) of health risks related to the testing of Agent Orange and other unregistered herbicides at CFB Gagetown June 14-16, 1966, and June 21-24, 1967.
DND has also used other (registered) herbicides at CFB Gagetown and across Canada since the 1950s. This broader use of registered herbicides will be reviewed over the next several years and relevant health information will be provided separately in the future. Although this document focuses on the testing of unregistered herbicides at CFB Gagetown June 14-16, 1966, and June 21-24, 1967, parts of this document would also be relevant to the discussion of potential health effects from chemical exposures in general (see especially "Under what circumstances might Agent Orange or its ingredients lead to health effects?" ).
- General Information
- Health Effects
- What health effects are associated with Agent Orange?
- What is the difference between an "association" and a "cause"?
- What are chance, bias, and confounding?
- Under what circumstances might Agent Orange or its ingredients lead to health effects?
- What are the health risks associated with large exposures to TCDD?
- Have Vietnam veterans in general been harmed by Agent Orange?
- Have Army Chemical Corps Vietnam veterans been harmed by Agent Orange?
- Have Air Force Ranch Hand Vietnam veterans been harmed by Agent Orange?
- Why have disability pensions been awarded in the US and Canada for illnesses associated with Agent Orange?
- Fate in the Environment
- Health Effects From Spraying in Gagetown
- How much Agent Orange was sprayed at CFB Gagetown?
- What is the health risk for CF members who were exposed to Agent Orange and Agent Purple at CFB Gagetown?
- Has the health of CF members living in PMQs or in communities near CFB Gagetown been affected by Agent Orange?
- I know of people in the communities near CFB Gagetown who are sick or dying - isn't this due to Agent Orange?
- What about other herbicides used at CFB Gagetown that contained some of the same ingredients as Agent Orange?
- What can I do to know more?
- Resources And References
The U.S. military used several different herbicide mixtures during the Vietnam War. These mixtures contained herbicides that were commercially available in the 1960's, but the mixtures themselves were made specifically for the U.S. military. In order to readily identify these different mixtures in the field, the storage drums for these mixtures used in Vietnam were painted with coloured bands, such as pink, purple, blue, white, green, and orange. The herbicide in the orange drums was an equal mixture of 2,4-D and 2,4,5-T (2,4-dichlorophenoxyacetic acid and 2,4,5-trichlorophenoxyacetic acid). It became known as "Agent Orange", as this was the colour of the bands on the drums it was stored in. In Vietnam, more than 45 million liters of Agent Orange were sprayed (the most of any herbicide formulation) and less than 2 million liters of Agent Purple were sprayed during the war (Stellman et al., 2003).
Both Agent Orange and Agent Purple were 50-50 mixtures of 2,4-D and 2,4,5-T; the distinction is in the type of 2,4,5-T. Agent Orange was a 50-50 mixture of n-butyl ester 2,4-D and n-butyl ester 2,4,5-T. Agent Purple contained 50% n-butyl ester 2,4-D, 30% n-butyl ester 2,4,5-T, and 20% isobutyl ester 2,4,5-T.
TCDD is an abbreviation for 2,3,7,8-tetrachlorodibenzo- p -dioxin (which can also be abbreviated as 2,3,7,8-TCDD). TCDD was an unintended contaminant in the production of 2,4,5-T. Therefore, TCDD was also a component of herbicide mixtures containing 2,4,5-T, such as Agent Orange. According to the U.S. Institute of Medicine, " TCDD is thought to be the most toxic of the compounds " used in Vietnam (Institute of Medicine, 2005).
TCDD is one specific type of chemical from a family of chemicals known as "dioxins". Some of the chemicals within the dioxin family are considered to be toxic whereas others are much less toxic. TCDD is considered to be the most toxic of the dioxins. Because of this, the toxicity of mixtures of dioxins is usually described in relation to TCDD. The scientific term for this is "toxic equivalent", or TEQ: the toxicity of a mixture of dioxins, expressed as an amount of TEQ, is comparable to the toxicity of the same amount of pure TCDD.
In later parts of this document ( "Is Agent Orange the only source of TCDD?" and "Can TCDD be measured in our bodies" ), some of the cited references discuss amounts of TEQ and amounts of TCDD. For simplicity, only the term "TCDD" is used in those sections.
The term "part per million" is used to describe the concentration of one substance (the "part") contained within another substance (the "per million"). Using the example of 2 ppm TCDD contamination, every million parts of Agent Orange would contain 2 parts of TCDD. If the TCDD contamination were 2 ppm, then a 55-gallon drum of Agent Orange would contain 4 drops of TCDD. If the TCDD contamination were 47 ppm (such as an Agent Purple sample), a 55-gallon drum of Agent Purple would contain about one third of a one-ounce shot glass of TCDD.
A part per trillion is a very tiny amount. One ppt is equivalent to 1 second in about 32 000 years, 1 drop of water in 40 Olympic size swimming pools, or the distance of 1 centimeter (the width of your "pinkie" fingernail) in 1200 round trips between Fredericton and Vancouver.
It is not known with certainty how much TCDD was in the Agent Orange and Agent Purple used by the United States during the Vietnam War. Because TCDD was an unintended contaminant, it was not routinely measured at the time these herbicide mixtures were made. However, the TCDD content can be estimated from samples collected from these herbicides. A survey of 15 million pounds of Agent Orange (200 samples) conducted by the U.S. Air Force revealed that the average TCDD content of the mixture was 1.91 ppm (parts per million, equivalent to mg/kg), and 68% of the samples contained 0.5 ppm or less of TCDD (Kearney et al., 1973). Four saved samples of Agent Orange left over from testing at Eglin Air Force Base in Florida had a mean TCDD concentration of 2.4 ppm (range 0.04 to 6.4 ppm); an analysis of 490 Agent Orange samples from U.S. and Pacific inventories had an average concentration of 2 ppm (Young et al., 2004b). Recently, it has been suggested that these values are an underestimate, and that an average TCDD contamination of 13 ppm for Agent Orange may be more realistic (Stellman et al., 2003).
Less information is available for Agent Purple. In the testing of 200 Agent Orange samples mentioned above, the four highest TCDD values of 17, 22, 33, and 47 ppm were actually Agent Purple, and not Agent Orange (Stellman, 2003). One saved Agent Purple sample at Eglin Air Force Base contained 45 ppm TCDD (Young et al., 2004b).
In 1991, because of uncertainty about the long-term health effects on Vietnam veterans of herbicide exposure, the U.S. Congress passed legislation that enabled the National Academy of Sciences' (NAS) Institute of Medicine (IOM) to perform a comprehensive evaluation of scientific and medical information regarding the health effects of exposure to Agent Orange.
In response to this legislation, the IOM conducts and publishes extensive reviews of scientific evidence regarding associations between health outcomes and exposures to TCDD and other chemical compounds in herbicides used in Vietnam. The IOM is widely considered to be the definitive source for medical information related to Agent Orange (Frumkin, H., 2003).
The IOM's most recent publication is "Veterans and Agent Orange: Update 2004" (http://www.iom.edu/report.asp?id=25476). The IOM has identified several health outcomes that are statistically "associated" with exposure to Agent Orange. Based on the scientific evidence available, the IOM has not concluded that exposure is the actual "cause" of these health outcomes.
With respect to Agent Orange, the IOM concluded there was "sufficient evidence of an association" for five health outcomes:
- Chronic lymphocytic leukemia (CLL)
- Soft-tissue sarcoma
- Non-Hodgkin's lymphoma
- Hodgkin's disease
The IOM has also found "limited or suggestive evidence of an association" for another seven outcomes:
- Respiratory cancer (of lung and bronchus, larynx, and trachea)
- Prostate cancer
- Multiple myeloma
- Early onset transient peripheral neuropathy
- Porphyria cutanea tarda
- Type 2 diabetes
- Spina bifida in the children of veterans
According to the IOM, the designation "limited or suggestive" means that the scientific evidence of an association is limited because chance, bias and confounding could not be ruled out with confidence.
The vast majority of the associations noted above have only been observed in studies of heavily-exposed populations, such as workers involved in chemical manufacturing or who have applied herbicides for many years. The IOM states " many conclusions regarding associations between exposure to TCDD or herbicides and diseases are based on studies of people exposed in occupational and environmental settings rather than on studies of Vietnam veterans ".
As mentioned above (see " What health effects are associated with Agent Orange? "), the IOM has identified illnesses that are statistically associated with exposure to herbicides, but the IOM has not determined that herbicide exposure is the cause of any illnesses. The distinction is based on the quality of scientific evidence. According to the IOM, " factors such as consistency of evidence, biological plausibility, temporality, dose-response, and strength of association may be considered when deciding whether an observed statistical association is actually causal" . For evidence from scientific studies, if the findings between different studies are not the same, or if the connections between exposure and outcomes are not very strong, or if other potential causes of the illness have not been taken into account, or if there are problems in the way the study was designed, then the scientific evidence is too weak to conclude that an exposure is the cause of a health effect, even though an association may exist.
Chance refers to "the luck of the draw". To use a practical example, consider flipping a coin. Each time that the coin is flipped, there is an equal chance of it coming up heads or tails. If you flip "heads" 5 times in a row, that may be unusual, but it may simply be due to chance (if you flipped the coin 1000 times in a row, for example, a run of 5 "heads" in a row may occur on a number of occasions). Alternatively, if you flipped the coin 1000 times and it came up "heads" every time, it would be highly unlikely that this pattern would be due to chance and you may suspect that there is another explanation for this observation (some sort of "rigged" coin, perhaps one that has "heads" on both sides). What if the coin came up "heads" 10 times in a row? Without knowing for certain if the coin was "rigged", would you feel confident in concluding that your observation was not due to chance? If an association is observed between an exposure and an outcome, scientific study is required to determine if the observation is a "real" association, or simply due to chance. Scientific study relies on statistics to exclude chance. If a finding is "statistically significant", then it is unlikely that chance is the reason for the finding.
Bias refers to a systematic error in the design or conduct of a study. Continuing the coin example, suppose you flipped the coin and recorded the results each time. However, you only recorded the result when the coin came up "heads" and never recorded it when the coin came up "tails". After a while, you may notice from your recorded results that you have 100 "heads" in a row, but no "tails". If you then concluded that the coin was "rigged", this would be an incorrect conclusion because your observations were biased. Scientific studies must be carefully designed, conducted, and analyzed so as to ensure that there are no biases that may lead to false conclusions.
Confounding occurs when in addition to the specific exposure and the outcome that are being studied, there is an another factor related to both the exposure and the outcome. For example, perhaps it is observed that after eating roasted marshmallows, itchy bumps appear on the skin. These bumps may last for a few days and then go away, but they reappear after eating roasted marshmallows again. One may then conclude that eating roasted marshmallows is the cause of the itchy bumps on the skin. However, if you are roasting marshmallows, you are likely doing this outside, when the weather is nice, and mosquitoes are present. While you are roasting marshmallows, mosquitoes are also biting you, which is the real cause of the itchy bumps on the skin. In this example, the mosquitoes would be a confounding factor.
In order for a health effect to be potentially caused by a chemical, several things must happen.
Firstly, an exposure to the chemical must have occurred. "Exposure" means that the chemical entered one's body, usually through inhalation, ingestion, or skin contact. For example, a person walking past a large sealed barrel of Agent Orange would not receive any exposure, and so the risk of any possible health effects from Agent Orange would be zero.
Secondly, the exposure must be of sufficient dose (amount). A central principle of toxicology is the concept of dose-response: at increasing levels of exposure to a harmful substance, health effects become more frequent and/or more severe. For example, consider the use of a painkiller medicine such as morphine. If the prescribed amount is taken, pain will be relieved with minimal side effects. However, if too much morphine is taken, it can lead to breathing problems and death. The only difference between these two scenarios is dose - it is the dose that makes the poison. It is important to consider that we are all exposed to small amounts of TCDD every day, mostly through the food we eat (see " Is Agent Orange the only source of TCDD? " and " Can TCDD be measured in our bodies? "). At present, scientific knowledge cannot determine a specific level of TCDD exposure at which a health effect will occur. The scientific study of TCDD can only determine the level of risk for health effects given a certain exposure to TCDD. The health risk from TCDD exposure will depend on the dose received. At very low doses of TCDD, the risk of health effects is very low and not detectable, but the risk increases as the dose of TCDD increases. For more discussion on "background" TCDD exposure and the amount of TCDD exposure that is associated with increased risks for health effects, please see " Is Agent Orange the only source of TCDD? ", " Can TCDD be measured in our bodies? ", and " What are the health risks associated with large exposures to TCDD? ").
Thirdly, the health effect in question must be associated with the chemical exposure. For example, we know that too much sun exposure is associated with an increased risk of skin cancer. If someone with a great deal of sun exposure develops emphysema (a lung disease), we would not attribute this lung condition with sun exposure, simply because there is no association between sun exposure and lung disease. The IOM has found evidence of an association between Agent Orange and several illnesses (see " What health effects are associated with Agent Orange? "). The IOM has also noted that several scientific studies have not shown any association with some other health problems, such as brain or gastrointestinal cancers. In other words, these cancers have never been associated with any amount of exposure. Therefore, if someone who was exposed to Agent Orange developed brain cancer, current scientific evidence indicates that it would be unlikely that the brain cancer was due to Agent Orange.
In conclusion, before a health effect can be considered to be associated with any substance, 1) there must be exposure, with the substance somehow having gotten inside a person, 2) the exposure must have been of a sufficiently large dose, or amount, to meaningfully increase the risk of a harmful effect (see " What are the health risks associated with large exposures to TCDD? ") and 3) the health effect in question must be scientifically associated with exposure to the substance. Unless these three criteria are satisfied, there is no medical or scientific reason to suspect that a health effect is due to the substance.
The adverse health effects associated with Agent Orange are believed to be due to TCDD, which current scientific evidence indicates to be carcinogenic. In other words, sufficient exposure to TCDD under certain conditions is believed to result in an increased risk of developing certain types of cancer. The human evidence that TCDD is carcinogenic is largely based on studies of highly exposed groups of industrial and agricultural workers (Pohl et al., 2002).
For example, one of the largest and most highly exposed industrial groups was made up of 5132 workers at 12 U.S. plants that produced chemicals contaminated with TCDD (Steenland et al., 1999). It was only the workers with the highest cumulative exposure to TCDD that had a greater risk of dying from all cancers combined, as compared with the U.S. general population. In this study, the degree of cumulative exposure depended on the level of TCDD contamination of the manufactured chemicals. For example, to reach the level of exposure of the workers in the highest exposure group, for whom the elevated cancer risk was observed, workers would have to be exposed to a chemical containing 10 ppm TCDD for their entire shift every working day for about 8 years. At a higher TCDD contamination level of 50 ppm, workers would have to be exposed for the entire shift every working day for about 1.5 years to reach the same level of exposure. It was noted that " excess cancer was limited to the highest exposed workers, with exposures that were likely to have been 100 to 1000 times higher than those experienced by the general population " (Steenland et al., 1999).
The magnitude of the increased risk of death from all cancers combined was 1.6 (Steenland et al., 1999). This means that compared to the general population, these highly exposed workers were 1.6 times more likely to die of cancer than the general population (in scientific terms, this comparison is referred to as a "standardized mortality ratio"). The results of this study were consistent with other research into the cancer risks associated with TCDD. A recent scientific review article noted that " a number of large-scale retrospective cohort mortality studies have found significant increases in cancer mortalities (all types of cancer combined). These increases were typically found in workers exposed to the highest levels of dioxin [TCDD] and in workers with the longest follow-up periods. In general, the standardized mortality ratios were low (less than 1.5); however, the high degree of consistency between studies suggests that the increases in mortalities were not due to chance " (Pohl et al., 2002).
For illnesses other than cancer, a recent scientific review article indicates that the evidence from human studies has not been strong enough (for example, the results are inconsistent or the studies are not designed well enough) to estimate specific risks associated with TCDD exposure. A more detailed discussion can be found in the article, which concludes that " although more than a dozen different adverse effects have been reported in various studies of humans in the past 25 years, the most consistent clinically important adverse effect of human exposure appears to be chloracne " (Greene et al., 2003). Chloracne is a skin condition. Typically, this condition is only observed in people when the TCDD level in their blood is several thousand times greater than the levels typically seen in the general population (Greene et al., 2003; Hays et al., 2003).
Veterans involved in herbicide handling and spraying in the Vietnam War were exposed to a number of different herbicide formulations (see "What is Agent Orange? "). Health studies of these veterans therefore look at the potential long-term health effects of herbicide exposures in general. These exposures were mainly to Agent Orange, but exposure to other herbicide formulations, such as Agent Purple, also occurred.
In comparison to heavily exposed industrial workers, Vietnam veterans were generally exposed to lower levels of TCDD. It is estimated that t he maximum TCDD dose experienced even by the US Air Force personnel directly involved in spraying ("Ranch Hand" veterans) was about one tenth of the maximum predicted dose of industrial workers (Akhtar et al., 2004).
The most recent study of death among U.S. Army veterans in general concluded that death rates due to chronic conditions, such as cancer or heart disease, were no different in veterans who served in Vietnam as compared to non-Vietnam veterans (Boehmer, 2004).
For the vast majority of Vietnam veterans, unless they were directly involved in the handling and spraying of Agent Orange, their exposure to Agent Orange would have been very small (Young et al., 2004a; Young et al., 2004c). A serum TCDD study of US Army Vietnam veterans who served as ground troops concluded that " most US Army ground combat troops who did not handle or spray herbicides were not heavily exposed to TCDD in Vietnam " (CDC, 1988). The greatest degree of Agent Orange exposure in Vietnam would have occurred among those veterans who directly handled or sprayed Agent Orange: Army Chemical Corps personnel and Air Force Operation Ranch Hand personnel.
Army Chemical Corps veterans were involved in the storage, preparation, and application of a variety of herbicides in Vietnam. In a recent study, the death rate among Vietnam Army Chemical Corps veterans was not significantly different than non-Vietnam veterans for all causes, circulatory disease, or cancer. Vietnam veterans in this group had a higher risk of dying due to digestive system diseases, largely cirrhosis of the liver, as compared to non-Vietnam veterans. The authors noted, however, that their study design did not account for lifestyle factors that can also cause cirrhosis of the liver, such as alcohol use: " it is possible that heavier drinking among the Army Chemical Corps Vietnam veterans than among their non-Vietnam counterparts could account for the excess deaths from cirrhosis of the liver " (Dalager et al., 1997). The Vietnam veterans' risk of death from digestive system diseases, including cirrhosis of the liver, was not higher than the risk for the general U.S. population (Dalager et al., 1997).
The aerial spraying of herbicides in Vietnam was conducted under the name "Operation Ranch Hand", from 1962 to 1971. U.S. Air Force veterans who took part in Operation Ranch Hand handled and sprayed herbicides, and they are the Vietnam veterans with the greatest exposure to Agent Orange. These veterans have been studied closely in the Air Force Health Study, the purpose of which was to determine if the health of veterans who handled and sprayed herbicides in Vietnam had been harmed by this exposure. The Air Force Health Study was launched in 1980 and t he most recent and reportedly final report was released in July 2005 (see http://www.brooks.af.mil/AFRL/HED/hedb/default.html , click on "Reports" in the left margin, and then select "2002 Follow-up Examination Results: May 2002 to March 2005" to access the full report).
The Air Force Health Study examined more than 300 health-related outcomes in these veterans, grouped broadly into 12 areas. The overall significant findings in each area can be found in the executive summary of the 2005 report and are summarized below.
General Health: Measures of general health were not related to herbicide exposure. The one exception was that body mass index (a crude measure of body fat) was greater with increasing blood TCDD levels. It was noted that this possibly reflected " the pharmacokinetics of dioxin [TCDD] elimination " (higher body fat levels slow down the removal of TCDD from the body - as body fat increases, blood TCDD increases, but TCDD does not cause higher body fat).
Cancer: Mixed patterns of associations were found, but no consistent or meaningful patterns that would suggest that herbicide exposure caused cancer. The report stated that " these patterns did not suggest an adverse relation between cancer and herbicide exposure" . [The enlisted ground crew, the sub-group with the highest TCDD exposure, had a decreased risk of cancer, but this was not statistically significant (in other words, chance could not be excluded as the reason for the decrease).]
Neurology: Of the many neurological tests that were performed, only differences in pinprick sensation and reflexes were observed in those with the highest TCDD exposure, providing " some support for a relation between dioxin [TCDD] exposure and peripheral nerve function ".
Psychology: No measures of psychological health were associated with herbicides or TCDD exposure.
Gastrointestinal: Of the many tests performed, there was no association between the gastrointestinal test results and herbicide or TCDD exposure. The only exception was a relation between TCDD and higher levels of triglycerides, a type of blood fat. Although measurable, this relationship was not considered to be of any health significance.
Skin: There was no evidence of chloracne (which is associated with TCDD exposure) in the Ranch Hand veterans.
Cardiovascular: A variety of health outcomes were studied, such as heart attacks, heart disease, vascular disease, strokes, and high blood pressure. The 2005 report concluded that " overall, cardiovascular health did not appear to be adversely associated with herbicide or dioxin [TCDD] exposure ".
Blood System: Several factors were measured in the blood of Ranch Hand veterans. Overall, there was no indication of an " adverse relation between herbicide or dioxin [TCDD] exposure and any haematological [blood disease] diagnosis ".
Kidneys: There was no indication of " adverse relation between renal [kidney] function and herbicide or dioxin [TCDD] exposure ".
Hormones (Endocrine System): There was a slightly increased risk of Type 2 (adult-onset) diabetes among the Ranch Hand veterans with the highest exposure. There were no consistent findings relevant to health for thyroid or sex hormones.
Immune System: There was no consistent association of health significance between any measure of immune function and herbicide or TCDD exposure.
Lungs: There was no association between lung health and exposure to herbicides or TCDD.
The 2005 Air Force Health Study report concluded that overall, only type 2 diabetes was associated with exposure to TCDD among these veterans with the greatest herbicide exposure. The Ranch Hand veterans were not more likely to be diagnosed with Type 2 diabetes than the comparison veterans without significant herbicide expsoure, but their risk of Type 2 diabetes increased with increasing blood TCDD level. The study confirmed associations between diabetes and other known risk factors: diabetes was more common in veterans who were older, who were obese, who smoked, and who had a family history of diabetes. The 2005 report noted that " the epidemiologic studies suggest that any increased risk of Type 2 diabetes from herbicide or dioxin [TCDD] exposure is small when compared to the known predictors - family history, obesity, physical inactivity - for diabetes ". The IOM has also found limited or suggestive evidence of a link between adult-onset (Type 2) diabetes and herbicides used in Vietnam, including Agent Orange, but concluded that other traditional risk factors for diabetes far outweigh the risks of Agent Orange.
The most recent study of causes of death among Ranch Hand Vietnam veterans was published in May 2005. Compared to Vietnam veterans who did not spray herbicides, Ranch Hand veterans did not have a greater risk of death due to cancer. When all Ranch Hand veterans were examined, the risk of death from all causes and from circulatory disease was slightly increased, but this was not statistically significant (in other words, chance could not be excluded as the reason for this slight increase). When only enlisted ground crew were examined, they had a slightly greater risk of death due to circulatory diseases than the comparison veterans. However, when veterans with serum TCDD measurements were examined, the risks of death from all causes, from cancer, or from circulatory disease were not significantly increased. In other words, those with measurable TCDD exposure did not have a greater risk of death from any cause compared to Vietnam veterans without significant herbicide exposure (Ketchum et al., 2005).
More information is available from the Air Force Health Study website ( http://www.brooks.af.mil/AFRL/HED/hedb/default.html - click on "Articles" in the left margin for a summary of all published scientific studies of Operation Ranch Hand veterans).
Why have disability pensions been awarded in the US and Canada for illnesses associated with Agent Orange?
As a result of political and policy decisions, the US Veterans Administration automatically presumes that veterans who served in Vietnam were exposed to Agent Orange (http://www.va.gov/pressrel/aoiss400.htm). They are also required by law to presume that, if a veteran develops an illness that is among those associated with Agent Orange, the illness is related to military service (Section 2, US Agent Orange Act of 1991, Public Law No. 102-4). The IOM notes that they have not found that Agent Orange is the cause of any illness, that the associations they found were largely based on studies of heavily-exposed chemical and agricultural workers, and that their conclusions " are not intended to imply or suggest policy decisions ".
Veterans Affairs Canada grants pensions for service-related disabilities, with the pension process designed to give applicants every chance to show how their disability is related to military service. Veterans Affairs Canada requires evidence of exposure and a medical diagnosis of the condition (ie. illness, injury or disease) that the applicant believes is related to the exposure. Pension Adjudicators take into account the latest scientific evidence available to establish an association between the condition and exposure to Agent Orange during service. Pension Adjudicators have flexibility in weighing the evidence presented in individual cases and, in the absence of credible evidence to the contrary, any doubt that arises in weighing evidence regarding a service-related illness associated with exposure is resolved in the applicant's favour. In fact, the Department is obliged, under the Pension Act, to give the "benefit of the doubt" to the Veteran.
The environmental fate of Agent Orange has been described in a recent review article (Young et al., 2004a). For Agent Orange to be as effective a herbicide as possible, the maximum amount of spray had to reach the vegetation as quickly as possible. To achieve this, aircraft flew very close to the treetops in calm weather conditions to minimize the amount of spray drifting outside of the target area. Rapid settling of the spray droplets was also important. The spray system used during the Vietnam War used spray nozzles designed to produce a droplet size of 320 to 350 m m (over 98% of the droplets produced were greater than 100 m m). Droplets of this size generally fall rapidly. Tests at Eglin Air Force Base in Florida showed that 87% of sprayed herbicides hit the vegetation within one minute (the remaining 13% took longer to settle due to vortices at the wing tips, drift, or evaporation). US studies showed that even the droplets smaller than 100 m m would have hit the vegetation less than 3 minutes after spraying (Young et al., 2004a).
For spray drift beyond the target area to occur, herbicide would have to remain in the air for extended periods of time, where it would be rapidly degraded by sunlight. Aerial photographs of herbicide-sprayed areas in Vietnam show very distinct and sharp lines between treated (dead) and untreated (healthy) trees. Had there been significant drift either way from the swath of aerial spraying, traces of damage would have been visible as streaks of discoloured foliage (Young et al., 2004a).
The studies showed that little aerially-sprayed Agent Orange reached the forest floor as liquid droplets. In relatively undisturbed dense forests, the forest canopy intercepted 87-97% of the sprayed herbicide. Vegetation below the forest canopy also took up some of the spray, such that the underbrush or forest floor received about 1-6% of the total aerial spray. The Agent Orange that lands on plant surfaces is absorbed into the wax layer of the plant cuticle within minutes and cannot be physically dislodged (Young et al., 2004a) . Agent Orange left on the plant surface breaks down in sunlight within hours (Crosby et al., 1977). It is estimated that very little, if any, Agent Orange can be dislodged from the plant surface 24 hours after spraying (Young et al., 2004a). It is likely that due to the degradation by sunlight of TCDD on leaf surfaces that little material would be left by the time the leaves fall to the ground.
The main contaminant of concern in Agent Orange was TCDD. TCDD is not very soluble in water and binds tightly to soil particles. Estimates of the half-life of TCDD (the amount of time it will take for the concentration of TCDD to be reduced by half) on the soil surface range from 9 to 15 years, whereas the half-life in subsurface soil may range from 25 to 100 years (ATSDR, 1998). Because of tight binding to soil particles, TCDD is unlikely to leech into underlying groundwater (ATSDR, 1998). However, TCDD may enter surface water secondary to soil erosion and runoff. Although some of the TCDD that makes its way to surface waters will be broken down by sunlight or evaporate, most will remain strongly attached to small particles of soil or organic matter and eventually settle to the bottom. TCDD attached to this organic matter may enter the aquatic food chain. Small aquatic organisms absorb TCDD that is attached to sediment and organic matter in bodies of water. Larger fish then consume these smaller organisms and accumulate TCDD in their fatty tissues. Human consumption of contaminated fish is thus a potential route of exposure (ATSDR, 1998).
Root uptake and translocation to upper plant parts is very minimal. The ATSDR described a laboratory study in which plants were grown in soil heavily contaminated with TCDD: " the amount of 2,3,7,8-TCDD applied to these soils was many thousands of times greater than that which would occur in soils from herbicide applications containing a few ppm 2,3,7,8-TCDD as an impurity. Even upon exposure to these high concentrations in the soil, significant amounts of 2,3,7,8-TCDD could not be measured in plants " (ATSDR, 1998). The vast majority of TCDD found in plants is due to absorption of airborne TCDD that settles on the plant surface. This has been demonstrated in studies of fruits and vegetables that show TCDD concentrations in the outer peel that are up to ten times greater than the TCDD concentration in the pulp (ATSDR, 1998).
Herbicide testing was conducted at Eglin Air Force Base in Florida from 1962 to 1970, when roughly 75 000 kg of 2,4-D and 76 000 kg of 2,4,5-T (the ingredients of Agent Orange) were aerially sprayed on an area of less than 3 square kilometres. It is estimated that 3.1 kg of TCDD contaminant was released in this area. Because of the extent of the testing, each hectare on the Eglin test grid received at least 1300 times more TCDD than a hectare sprayed with Agent Orange in Vietnam. Much of the vegetation on the test site had been removed, allowing an opportunity to study ground-based residues that would not be affected by interception of the sprayed herbicides by the forest canopy (Young et al., 2004b).
Small but detectable levels of TCDD (in the parts per trillion range) were found in some soil samples 20 years after the last application of herbicide. It was estimated that the vast majority of TCDD that reached the ground had been degraded by sunlight within 24 hours of spraying and would not have persisted in the environment. For the small amounts of TCDD that were detected, the majority of TCDD was confined to the top 15 cm of soil, indicating that there was little travel of TCDD deeper into the soil. In the years that followed the herbicide testing, vegetation growth gradually returned to normal, indicating that there was no persistent herbicide effect. Examination of animal species that lived in close contact with the soil did not reveal significant health effects (Young et al., 2004b).
In summary, very large quantities of herbicides were applied to the Eglin Air Force Base test site, far more than would be applied during typical aerial spraying, and far more that were used during the herbicide tests at CFB Gagetown June 14-16, 1966, and June 21-24, 1967 (see " How much Agent Orange was sprayed at CFB Gagetown? "). These herbicides were applied over areas where vegetation had been removed, thereby maximizing the amount of herbicide that reached the ground. No long-term negative effects on vegetation or wildlife were detected. Although TCDD could be detected in the soil years after the testing, the amounts present were extremely small and did not appear to have a significant adverse effect on the environment (Young et al., 2004b).
Agent Orange is not a significant source of TCDD in the environment. Most of the TCDD released into the environment comes from combustion sources, such as municipal and medical waste incineration, backyard burning of household waste such as plastics, cement kilns, forest and brush fires, and burning of fuel for agricultural purposes and home heating. TCDD can be formed in metals operations, such as aluminum smelting, steel production and scrap metal recovery. TCDD can also be formed as a byproduct in the manufacture of chlorine-bleached wood pulp and chlorinated chemicals (ATSDR, 1998; Hays et al., 2003; Sullivan et al., 2001; Travis et al., 1991).
Because of this past and continued production and release of TCDD, it is everywhere in our environment in very small quantities. Everyone is exposed to small amounts of TCDD every day, mostly through food (Birmingham et al., 1989; Gilman et al., 1991; Travis et al., 1991; Huwe, 2002). Cigarette smoke is also an important source of exposure (Muto et al., 1989). It has been estimated that the average Canadian or American adult takes in about 40-150 picograms of TCDD every day (ATSDR, 1998; Health Canada, 1994; Gilman et al., 1991). A gram is a relatively small amount: one teaspoon of water weighs about 5 grams and there are 450 grams in one pound. A picogram is a trillionth of a gram. Put another way, one picogram is one part per trillion of a gram (see "How much is a part per trillion (ppt)?" ). Therefore, 40 to 150 picograms of TCDD is a very small amount, but it is equivalent to about 100 billion molecules of TCDD (see " Calculation "). Every day, the average adult is exposed to about 100 billion molecules of TCDD.
In a study of industrial workers for whom an elevated cancer risk was observed (see " What are the health risks associated with large exposures to TCDD? "), it was noted by the authors that " excess cancer was limited to the highest exposed workers, with exposures that were likely to have been 100 to 1000 times higher than those experienced by the general population " (Steenland et al., 1999).
Recently, the World Health Organization (WHO) established a tolerable daily dioxin intake equivalent to 1 to 4 picograms of TCDD per kilogram of body weight per day ( http://www.who.int/mediacentre/factsheets/fs225/en/print.html ), which is similar to other international health assessments (Pohl et al., 2002). Health Canada's tolerable daily intake value is currently under review, but will likely be equivalent to the WHO value. Based on the assessment of health authorities, the tolerable daily intake is the amount of TCDD that people can be exposed to every day of their lives without harm. The tolerable daily intake is expressed in a manner that takes into account differences in body weight between different people. For example, the tolerable daily intake of TCDD for a 70 kilogram adult is 280 picograms (4 picograms of TCDD per kilogram multiplied by 70 kilograms) per day. For a 80 kilogram adult, the tolerable daily intake would be 320 picograms (4 picograms of TCDD per kilogram multiplied by 80 kilograms) per day.
Because of continuous low-level exposure to TCDD, we all have measurable amounts of TCDD in our bodies, referred to as a "background" level of TCDD. It is estimated that in North America, the average body burden of TCDD (the amount of TCDD contained within our bodies) is 3-7 parts per trillion (ppt), measured either in body fat or in blood lipids (Hays et al., 2003; Travis et al., 1991, ATSDR 1998).
In comparison, the average serum level of TCDD in a sample of Ranch Hand personnel (who handled and sprayed herbicides in Vietnam) was 49 ppt in 1987, many years after exposure had occurred. Because half the TCDD in our bodies is naturally eliminated every 7-12 years (TCDD's half-life), it was estimated that 2 to 4 half-lives had passed since the time of their exposure and that their serum TCDD levels around the time of exposure had probably been several hundred ppt (MMWR, 1988). Other Vietnam veterans who did not directly spray or handle herbicides in Vietnam had body burdens of TCDD that were no different than normal background levels, in the range of 2 to 4 ppt (Young et al., 2005). A serum TCDD study of US Army Vietnam veterans who served as ground troops concluded, " most US Army ground combat troops who did not handle or spray herbicides were not heavily exposed to TCDD in Vietnam " (CDC, 1988).
It is estimated that the maximum TCDD dose experienced by Ranch Hand veterans was only about one tenth of the maximum predicted dose of industrial workers (Akhtar et al., 2004). In a study of heavily exposed industrial workers (for whom evidence of associations between TCDD and cancer was observed), the average estimated serum level of TCDD at the end of exposure was 1589 ppt, with a maximum value of 210 054 ppt (Steenland et al., 2001). People who have serum TCDD levels greater than 12000 ppt develop a skin condition known as chloracne (Greene et al., 2003).
We are all exposed to TCDD. It can be measured in our bodies. The risk of health effects associated with TCDD is entirely dependent on the degree of exposure, or dose (see "Under what circumstances might Agent Orange or its ingredients lead to health effects?" ).
Agent Orange was one of a number of different herbicide mixtures tested at CFB Gagetown June 14-16, 1966, and June 21-24, 1967 . Several of these mixtures, including Agent Orange, contained the herbicide 2,4,5-T, which was potentially contaminated with parts per million of TCDD (see " How much TCDD did Agent Orange and Agent Purple contain? " for discussion). During the tests, records indicate that helicopters sprayed the herbicide in an unused and remote area of the base, not in proximity to any residential or working areas, under strictly controlled conditions, and with little to no wind. The total area sprayed by various herbicides containing 2,4,5-T (eg. Agent Orange, Agent Purple, and others) was 126.5 acres in 1966 and 12.0 acres in 1967, for a total of 138.5 acres, or about 0.6 square kilometres. The total amount of all herbicides containing 2,4,5-T that were sprayed during the 1966 and 1967 tests was 883 kg, of which 338 kg was Agent Orange and 267 kg was Agent Purple ( AD 843989 Technical Memo 141, 1968; AD 842825 Technical Memo 145, 1968). On average, 1.6 grams of herbicides containing 2,4,5-T were sprayed per square meter.
The greatest amount of herbicide exposure resulting from the June 14-16, 1966, and June 21-24, 1967 tests would likely have occurred among those people who directly handled or were sprayed by herbicides. In considering their health risks, it is important to consider the concept of dose-response (see "Under what circumstances might Agent Orange or its ingredients lead to health effects?" and "What are the health risks associated with large exposures to TCDD?" ). Most of the associations between TCDD exposure and health outcomes have been observed in heavily exposed industrial workers. Vietnam veterans with the greatest amount of herbicide exposure (Operation Ranch Hand veterans) had less overall TCDD exposure than heavily exposed industrial workers. Their long-term health outcomes are described above (see " Have Air Force Ranch Hand Vietnam veterans been harmed by Agent Orange?" ) . Personnel exposed to herbicides during June 14-16, 1966, and June 21-24, 1967 testing at CFB Gagetown would generally have had less exposure than Ranch Hand veterans, who on average spent more than a year in Vietnam (Akhtar et al., 2004).
Without knowing specific details of how the herbicides were handled during the June 14-16, 1966, and June 21-24, 1967 tests, subsequent activities that might have resulted in exposure, and the specific TCDD concentrations of the herbicides used, it is not possible to make definitive statements about the degree of potential exposure and health risks for particular individuals involved. Given the relatively small herbicide quantities applied, relatively brief duration of exposure, and the findings of health studies of more heavily exposed groups, the scientific evidence reviewed above suggests that the health risks would generally be lower than the risk for more heavily-exposed Vietnam veterans and lower still than the risk for the heavily-exposed industrial and agricultural workers on whom most of the Institute of Medicine associations are based.
With respect to CF members travelling through the targeted area after the spraying or conducting activities elsewhere in the training area, the evidence summarized above suggests that, in the absence of an unusual exposure incident, it is unlikely that they would have received a level of exposure significant enough to harm human health (Young et al., 2004a; CDC, 1988). (see "What happens to Agent Orange after it is sprayed?" and "What happens to Agent Orange after it lands on the ground?")
Has the health of CF members living in PMQs or in communities near CFB Gagetown been affected by Agent Orange?
The only study on the question of health effects of people living near CFB Gagetown was conducted in 1981 by Health and Welfare Canada and it looked at limited data and limited health information. In order to assess if the use of Agent Orange and other herbicides had resulted in detectable health effects in the communities surrounding CFB Gagetown, Sunbury County (which borders the area of CFB Gagetown where the June 14-16, 1966, and June 21-24, 1967 herbicide testing occurred) was the area chosen for study. Death rates due to all causes, circulatory diseases, and cancer were either lower or no different than expected (Wigle et al., 1981). Potential reproductive health effects were evaluated by studying the outcomes of babies born around the time of spraying and in the months that followed. The study concluded that the herbicide testing at CFB Gagetown " resulted in no significant increase of adverse pregnancy outcome events in the population adjacent to Camp Gagetown "(Wigle et al., 1981). The study also noted " Based on climatic conditions, spray technique, knowledge of the chemicals used and the results of other studies it is unlikely that persons outside the confines of Camp Gagetown would have received a significant exposure to any of the defoliants tested " (Wigle et al., 1981). DND is assessing what further health study may be required.
The evidence summarized above and what is currently known about the spraying suggest that it is unlikely that the herbicides sprayed at CFB Gagetown June 14-16, 1966, and June 21-24, 1967 would have travelled a significant distance beyond the target area or resulted in sufficient environmental contamination to harm human health (see "What happens to Agent Orange after it is sprayed?" and " What happens to Agent Orange after it lands on the ground?" ).
I know of people in the communities near CFB Gagetown who are sick or dying - isn't this due to Agent Orange?
Sufficiently great exposure to TCDD-containing herbicides could potentially increase the risk of illnesses associated with Agent Orange (see " Under what circumstances might Agent Orange or its ingredients lead to health effects?" and "What are the health risks associated with large exposures to TCDD ? " ).
Unfortunately, it is rare for anyone to live his or her entire life without any sort of health problem. The Public Health Agency of Canada contains a wealth of information on the burden of disease in Canada ( http://www.phac-aspc.gc.ca ). For example, by the middle of 2005, more than 35 000 Canadians had died of cardiovascular disease and more than 30 000 Canadians had died of cancer ( http://www.phac-aspc.gc.ca/ccdpc-cpcmc/index_e.html ). According to Diabetes in Canada Second Edition (2002), it is estimated that 30 000 Canadians die each year from diabetes and diabetes-related complications ( http://www.phac-aspc.gc.ca/publicat/dic-dac2/english/01cover_e.html ). According to Congenital Anomalies in Canada 2002, roughly 2 to 3% of babies in Canada are born with a serious congenital anomaly, usually with no family history or known risk factors ( http://www.phac-aspc.gc.ca/publicat/cac-acc02/index.html). According to Canadian Cancer Statistics 2005 (http://www.cancer.ca/ccs/internet/standard/0,,3172_14291__langId-en,00.html), the lifetime probability of developing cancer for males is 44% and for females is 38%. In other words, the average Canadian male has a 1 in 2.3 chance and the average female has a 1 in 2.6 chance of developing cancer in their lifetimes. Males have a 29% and females a 24% chance of dying from cancer in their lifetime; roughly one chance in four for the two sexes combined. It is estimated that in 2005, 448 out of every 100 000 men in Canada and 355 out of every 100 000 women will develop cancer. Roughly 149 000 Canadians will be diagnosed with cancer and 69 500 Canadians will die from cancer in 2005.
In New Brunswick, it is estimated that 3 900 people will be diagnosed with cancer and 1 800 people will die of cancer in 2005. In order to compare these numbers for New Brunswick with the rest of Canada, it is necessary to look at standardized cancer rates, which take into account differences in age and population size between provinces. The rates of new cancer diagnoses and cancer deaths in New Brunswick are higher than the Canadian average, but the New Brunswick rates are generally the lowest of the Maritime Provinces (Canadian Cancer Statistics, 2005).
There are many potential causes and risk factors for the illnesses that affect Canadians. Of all the people who have or will develop these illnesses, few have been exposed to Agent Orange or Agent Purple.
What about other herbicides used at CFB Gagetown that contained some of the same ingredients as Agent Orange?
A total of 251 products containing 2,4,5-T, which contained TCDD contamination, were registered for use in Canada between 1948 and 1981. The last product was registered in 1981, but thereafter the registration of all of these products was discontinued. For information on 2,4-D, which is still registered for use in Canada, see the following Health Canada website: http://www.pmra-arla.gc.ca/english/consum/2,4-DFAQ-e.html .
DND's use of herbicides will be reviewed over the next several years. Some of the health information noted above would also generally apply to other chemical exposures, in that the risk for adverse health effects would depend on the dose and duration of exposure (see especially "Under what circumstances might Agent Orange or its ingredients lead to health effects?" ).
Talk to your MO and look at these or any other references for yourself. If you do not see a web link to a reference you would like, ask your MO for a copy and an explanation of any technical language or concepts that are not clear to you. Although there are many other sources of information, the references consulted are trusted by the Surgeon General, are believed to be based on sound scientific evidence and analysis, and are believed to represent the general consensus about Agent Orange in the medical and scientific community. Do not hesitate to consult your MO if you have questions about this or any other health concern.
(See discussion in " Is Agent Orange the only source of TCDD? ")
- average daily TCDD intake estimates: 47 pg/day (ATSDR, 1998); 39-147 pg/day (Health Canada, 1994; Gilman et al., 1991): assume 50 pg/day daily intake
- 1 pg = 10 -12 g
- molecular weight of TCDD = 321.96 g/mol
- Avagadro's number = 6.022 x 10 23
50 pg/day) x (10 -12 g/pg) x (1 mol/321.96 g) x (6.022 x 10 23 molecules/mol
= 9.35 x 10 10 molecules/day (93 500 000 000 molecules per day)
U.S. Institute of Medicine
- Veterans and Agent Orange 2004 Update: http://www.iom.edu/report.asp?id=25476
U.S. Air Force Health Study
- http://www.brooks.af.mil/AFRL/HED/hedb/default.html (click on "Articles" in the left margin for a summary of all published scientific studies of Operation Ranch Hand veterans; click on "Reports" in the left margin, and then select "2002 Follow-up Examination Results: May 2002 to March 2005" to access the most recent report )
U.S. National Agricultural Library special collection on Agent Orange:
- It's Your Health": http://www.hc-sc.gc.ca/iyh-vsv/environ/dioxin_e.html
Health Canada's Pest Management Regulatory Agency
- Information on 2,4-D and other herbicides: http://www.pmra-arla.gc.ca/
Agency for Toxic Substances and Disease Registry (ATSDR)
- Public Health Statement: http://www.atsdr.cdc.gov/toxprofiles/phs104.html
World Health Organization
- Fact Sheet: http://www.who.int/mediacentre/factsheets/fs225/en/print.html
U.S. Environmental Protection Agency (US EPA)
- Questions and answers: http://www.cfsan.fda.gov/~lrd/dioxinqa.html
- Dioxin exposure and health: http://europa.eu.int/comm/environment/dioxin/
AD 843989 Technical Memorandum 141: Defoliation Tests in 1966 at Base Gagetown, NB, Canada" authored by Kenneth D. Demaree and Richard A Creagar, October 1968. Department of the Army, Fort Detrick, Frederick, Maryland.
AD 842825 Technical Memorandum 145: "Chemical Defoliation of Northern Tree Species" authored by Kenneth D. Demaree and Richard A Creagar, October 1968. Department of the Army, Fort Detrick, Frederick, Maryland.
Akhtar, F.Z., Garabrant, D.H., Kethcum, N.S., et al. Cancer in US Air Force veterans of the Vietnam War. Journal of Occupational and Environmental Medicine 2004; 46: 123-136.
ATSDR (Agency for Toxic Substance and Disease Registry) Toxicological profile for Chlorinated dibenzo- p -dioxins (CDDs) U.S. Department of Health and Human Services, Agency for Toxic Substances and Disease Registry, Atlanta, Ga. 1998.
Birmingham, B., Gilman, A., Grant, D., et al. PCDD/PCDF multimedia exposure analysis for the Canadian population: detailed exposure estimation. Chemosphere 1989; 19: 637-642.
Boehmer, T.K.C., Flanders, D., McGeehin, M.A., et al. Postservice mortality in Vietnam veterans: 30-year follow-up. Archives of Internal Medicine 2004; 164: 1908-1916.
CDC (Centers for Disease Control). Serum 2,3,7,8-t etrachlorodibenzo- p -dioxin levels in US Army Vietnam era veterans. JAMA 1988; 260: 1249-1254.
Crosby, D.G., Wong, A.S. Environmental degradation of 2,3,7,8-tetrachlorodibenzo- p -dioxin (TCDD). Science 1977; 195: 1337-1338.
Dalager, N.A., Kang, H.K. Mortality among army chemical corps Vietnam veterans. American Journal of Industrial Medicine 1997; 31: 719-726.
Frumkin, H. Agent orange and cancer: an overview for clinicians. CA: A Cancer Journal for Clinicians 2003; 53(4): 245-255.
Gilman, A., Newhook, R., Birmingham, B. An updated assessment of the exposure of Canadians to dioxins and furans. Chemosphere 1991; 23: 1661-1667.
Greene, J.F., Hays, S., Paustenbach, D. Basis for a proposed reference dose (RfD) for dioxin of 1-10 pg/kg-day: a weight of evidence evaluation of the human and animal studies. Journal of Toxicology and Environmental Health, Part B 2003; 6(2): 115-159.
Hays, S.M., Aylward, L.L. Dioxin risks in perspective: past, present, and future. Regulatory Toxicology and Pharmacology 2003; 37: 202-217.
Health Canada. Canadian health based soil quality criteria for contaminated sites: polychlorinated dibenzodioxins and polychlorinated dibenzofurans - supporting documentation. Prepared for the Canadian Council of Ministers of the Environment. May 1994.
Huwe, J.K. Dioxins in food: a modern agricultural perspective. Journal of Agricultural and Food Chemistry 2002; 50: 1739-1750.
Institute of Medicine (2005). Veterans and Agent Orange: Update 2004. Washington, DC: National Academy Press.
Kearney, P.C., Woolson, E.A., Isensee, A.R., et al. Tetrachlorodibenzodioxin in the environment: sources, fate, and decontamination. Environmental Health Perspectives 1973; 5: 273-277.
Ketchum, N.S., Michalek, J.E. Postservice mortality of Air Force veterans occupationally exposed to herbicides during the Vietnam War: 20-year follow-up results. Military Medicine 2005; 170: 406-413.
MMWR (Morbidity and Mortality Weekly Report). Serum 2,3,7,8-tetrachlorodibenzo- p -dioxin levels in Air Force Health Study participants - preliminary results. MMWR 1988; 37(20); 309-311.
Muto, H., Takizawa, Y. Dioxins in cigarette smoke. Archives of Environmental Health 1989; 44(3): 171-174.
Pohl, H.R., Hicks, H.E., Jones, D.E., et al. Public health perspectives on dioxin risks: two decades of evaluations. Human and Ecological Risk Assessment 2002; 8: 233-250.
Steenland, K., Piacitelli, L., Deddens, J., et al. Cancer, heart disease, and diabetes in workers exposed to 2,3,7,8-tetrachlorodibenzo- p -dioxin. Journal of the National Cancer Institute 1999; 91(9): 779-786.
Steenland, K., Deddens, J., Piacitelli, L. Risk assessment for 2,3,7,8-tetrachlorodibenzo- p -dioxin (TCDD) based on an epidemiologic study. American Journal of Epidemiology 2001; 154: 451-458.
Stellman, J.M., Stellman, S.D., Christian, S.D., et al. The extent and patterns of usage of agent orange and other herbicides in Vietnam. Nature 2003; 422: 681-687.
Sullivan, J.B., Kreiger, G.R. Clinical Environmental Health and Toxic Exposures. Philadelphia: Lippincott Williams & Wilkins, 2001.
Travis, C.C., Hattemer-Frey, H.A. Human exposure to dioxin. The Science of the Total Environment 1991; 104: 97-127.
Wigle, D.T., Mao, Y. Investigation of potential health effects due to defoliant spraying at Camp Gagetown, New Brunswick. Laboratory Centre for Disease Control, Health Protection Branch, Health and Welfare Canada. June, 1981.
Young, A.L., Giesy, J.P., Jones, P.D., et al. Environmental fate and bioavailability of Agent Orange and its associated dioxin during the Vietnam War. Environmental Science & Pollution Research 2004a; 11(6): 359-370.
Young, A.L., Newton, M. Long overlooked historical information on Agent Orange and TCDD following massive applications of 2,4,5-T-containing herbicides, Eglin Air Force Base, Florida. Environmental Science & Pollution Research 2004b; 11(4): 209-221.
Young, A.L., Cecil, P.F., Guilmartin, J.F. Assessing possible exposures of ground troops to agent orange during the Vietnam War: the use of contemporary military records. Environmental Science & Pollution Research 2004c; 11(6): 349-358.
Young, A.L., Regens, J.L. Serum TCDD levels and health effects from elevated exposure: medical and scientific evidence. Environmental Science & Pollution Research 2005; 12(1): 1-4.
Who Do I Contact? / Requests for Information
Do you have information about the use of herbicides at CFB Gagetown?
If you do, the Government of Canada encourages you to share that information and discuss your experience by participating in its Fact Finding Initiative.
The Government of Canada does not consider any information about the use of herbicides (including Agent Orange) at CFB Gagetown to be secret. Disclosure of this information will not be considered a breach of the Security of Information Act (formerly known as Official Secrets Act) or of any other obligation of confidentiality.
If you wish, the information you provide will be kept confidential (unless a court orders otherwise).
The information you provide will not jeopardize your:
- Canada pension plan;
- VAC disability pension; or
- Canadian Forces pension plan
Former Canadian Forces members, DND employees and civilian contractors should follow the steps outlined below if they feel they have suffered health problems stemming from exposure to Agent Orange:
Former and Current CF Members
Veterans Affairs Canada's mandate is to provide disability pension and health care services to Canadian Forces veterans who suffer a service-related illness or disability.
Former and still-serving Canadian Forces members who think they have a service-related illness are encouraged to contact Veterans Affairs Canada.
The Veterans Affairs Canada national referral numbers are 1-866-522-2122 (English) and 1-866-522-2022 (French). Information is also available on their website at http://www.vac-acc.gc.ca/.
Inquiries can also be made to the Centre for the Support of Injured and Retired Members and Their Families (The Centre) at 1-800-883-6094 or by visiting the Centre's website at www.forces.gc.ca/centre.
Former and Current Employees of the Department of National Defence
Current and former employees of National Defence who feel they may suffer from an occupational illness as a result of exposure to Agent Orange during the course of their employment may submit the details of their claim to the DND Civilian Human Resources Office in Gagetown. Current employees should submit their claims through their normal local management contacts to ensure that their claims are processed in the most efficient manner possible. Former employees should submit the details of their claim to:
Civilian Human Resources Office Atlantic Civilian Human Resources Service Centre Compensation Administrator CFB/ASU Gagetown P.O. Box 17000 Station Forces Oromocto, New Brunswick E2V 4J5
Instructions on the completion of claims and the forms can be found at the following website: http://www.whscc.nb.ca/forms_e.asp#frmwrk.
Former and Current Federal Government Employees
The Government Employees Compensation Act (GECA) provides compensation benefits to the employees of federal departments, agencies and Crown corporations for injuries and illnesses arising from their employment. It covers approximately 400,000 employees across Canada. Information on the GECA can be found on the Federal Workers' Compensation Service website at http://www.hrsdc.gc.ca/asp/gateway.asp?hr=en/lp/lo/fwcs/geca.shtml&hs=fxf.
The Minister of Labour and Housing has agreements with the ten provincial workers' compensation boards to adjudicate claims under GECA. Federal employees receive benefits based on the rates and conditions of the province where they are usually employed.
Compensation claims for employees working in New Brunswick should be forwarded to the Regional Injury Compensation Unit, Human Resources Skills Development Canada, in Moncton, New Brunswick, for transmission to the New Brunswick Workplace Health, Safety and Compensation Commission.
Their mailing address is:
1045 Main Street Moncton, New Brunswick E1C 9G8
Former and Current Civilian Contractor Employees
The Workplace Health, Safety and Compensation Commission of New Brunswick provides accident prevention services, occupational health and safety assistance and cost-effective disability and liability insurance to workers and employers in New Brunswick. It also administers pension benefits related to workplace accidents and workplace related illnesses.
Former and current employees of civilian contractors who believe that they may have been exposed to Agent Orange and Agent Purple during the 1966 and 1967 testing conducted at CFB Gagetown can apply for compensation to the Workplace Health, Safety and Compensation Commission of New Brunswick.
Queries should be referred to Mr. Omer Robichaud at (506) 738-4150.
Information can also be found on the New Brunswick Workplace Health, Safety and Compensation Commission website at http://www.whscc.nb.ca.
Based on the information we have to date, it is unlikely that civilians outside the base were exposed to Agents Orange or Purple as a result of this testing. Nevertheless, we understand and acknowledge the concerns expressed by some individuals. We take such concerns very seriously. DND will continue to work with key departments to research this issue and to communicate the information to concerned citizens in a timely fashion.
If there is evidence that civilians were exposed to Agents Orange and/or Purple during the testing in 1966 and 1967, the Government of Canada will deal with the issue.
The Government of Canada has also established a toll-free number to assist people with general inquiries related to this matter. The number is 1-866-558-2945 and it is operated from 8:00 a.m. to 4:30 p.m. (EST) daily, Monday to Friday.
Gagetown Range and Training Area
Frequently Asked Questions
What are dioxins?
Dioxins encompass a large family of about 200 chemicals. Certain types of dioxins (2,3,7,8-TCDD) are much more toxic than others and are classified as "dioxins of concern."
In the past, some herbicides were contaminated with dioxins. In light of emerging knowledge and concerns regarding dioxins, the manufacturing processes of herbicides have been improved to reduce or eliminate such contamination. In the case of 2,4-D for example, manufacturing processes were modified in the early 1980s to essentially eliminate contamination with dioxins of concern.
Is Agent Orange the same as any 50:50 mixture of 2,4-D and 2,4,5-T?
No. Agent Orange and other "Agent" chemicals were never registered for use in either Canada or the U.S. These "Agent" chemicals were manufactured specifically for the U.S. military. Some of the manufacturing processes of these military "Agent" chemicals were different than the manufacturing processes of registered herbicides. Production was accelerated to supply the U.S. military with the large quantities needed for use in Vietnam. There are reports that the accelerated manufacturing processes sometimes resulted in higher dioxin levels for Agents Orange and Purple than for registered herbicides of similar formulation.
Why are the dioxin levels in soil samples from Ripon Road and the Clones and Murphy Bivouacs not a concern if levels are much higher than the Canadian Council of Ministers of the Environment (CCME) guidelines?
The Canadian Council of Ministers of the Environment (CCME) soil quality guideline for dioxins of 4 parts per trillion is based on the average or background level of dioxins typically found in Canadian soils. The risks associated with background levels of dioxin in soil is considered to be minimal.
It is not uncommon to find levels across the country that are higher than the background levels. These higher levels can be from numerous sources, including forest fires and natural geological anomalies. However, when dioxin levels in soil are higher than average, it does not automatically mean that there would be a risk of adverse health effects. The key to determining whether there is any risk is to look at the combination of the dioxin level in the soil, how people might have been exposed and for how long they may have been exposed.
In the case of CFB Gagetown, a site-specific risk assessment was conducted to estimate the exposures that people could receive from the levels of dioxins measured in the soil. The independent contractor concluded that there is no increased risk of dioxin-related illness from living or working at CFB Gagetown today.
In the task 3A-2 report, it confirms that dioxins were detected in every single soil sample that was taken. Does this mean that the whole base is contaminated with dioxins?
As explained above, dioxins naturally occur in the environment and are released from many sources, including forest fires. They are often found in soils across Canada.
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