Sep 9, 2004
The following with supplied by the NZ Ministry of Health
1. What are dioxins?
Dioxins are a group of chemicals that share similar structures and ways of affecting the body. These compounds belong to three closely related
families – the polychlorinated dibenzo-p-dioxins, polychlorinated dibenzofurans (called furans), and certain polychlorinated biphenyls (PCBs). All
dioxins are very stable and unlike most other chemicals do not quickly decompose or break down in the environment. Some of them have demonstrated
adverse health effects in animals at very low levels. For this reason most countries are trying to reduce the amount of dioxin in the environment and
people’s exposure to them.
Seventeen dioxins are thought to pose a health and environmental risk. The toxicity (or level of harmfulness) of the 17 varies;
2,3,7,8-tetrachlorodibenzo-p-dioxin, abbreviated as 2,3,7,8-TCDD or TCDD and commonly referred to as dioxin, is the most toxic.
2. How do dioxins get into the environment?
There are a few natural sources of dioxins, such as forest fires and volcanic activity, but most dioxins are from man made sources and are largely the
result of formation as by-products of combustion (burning) and certain industrial processes. Advances in chemical and environmental management
practices since the late 1980s have resulted in a reduction in dioxins emissions in New Zealand.
In 2001, New Zealand became a signatory to the Treaty on Persistent Organo-Pollutants (POPs) the aim of which is to eliminate dioxin, where possible,
from the environment.
3. How do dioxins get into our body?
Some exposure to dioxins is inevitable since they persist in the environment and are formed naturally as well as by certain industrial processes. Cigarette smoke also contains small amounts of dioxins.
For most New Zealanders about 90 per cent of dioxin exposure is through diet, mainly from foods that contain animal fats such as meat, dairy products,
eggs and fish. Dioxins enter the food chain after being deposited onto soil and plant surfaces from the air and subsequently being eaten by grazing animals. Plants take up only very small amounts of dioxins via their roots. Small amounts of exposure occur from inhalation, skin absorption, and inadvertent ingestion of contaminated soil or dust.
Dioxins are broken down by exposure to sunlight, but if buried in the soil they are likely to remain there for a very long time. Once in the body dioxin accumulates in fat and persists for many years.
Typically lower levels of dioxins are found in people from less industrialised countries and in younger people. Levels for the New Zealand general population are at the low end of the range of levels reported internationally.
4. How much dioxin do we have in our bodies?
A study of the level of dioxin in the blood of 1834 New Zealanders conducted by the Ministry for the Environment found the average amount of dioxin in
blood was 3.5 pg/g (MfE, 2001) for people of the same age and sex as the Paritutu people tested. A picogram is a trillionth of a gram (0.000000000001g)
A study of the dioxins in the breast milk of a sample of New Zealand women, for the Ministry of Health, found the levels had decreased from an average of 16.4 pg/g of fat in breast milk in 1988 to 5.3 pg/g in 1998 – a fall of by about 70 per cent over the decade. The study of dioxins in breast milk was for all dioxins, not solely the TCDD dioxin found at elevated levels in the blood serum study.
5. What health effects are caused by exposure to dioxin?
Despite many studies much is still not known about how dioxin affects humans and at what level exposed individuals might be likely to have health effects. How much dioxin the person is exposed to and for how long is important as well as individual susceptibility.
The most well studied dioxin is TCDD. At very high doses it may cause a severe acne-like skin condition known as chloracne and cancer in some people.
The adverse health effects associated with TCDD exposure are not yet fully known. Animal studies show immune, reproductive and developmental effects.
Although the evidence of non-cancer effects in people is to date limited, these animal studies have been used internationally to establish health-based guidelines for exposure to dioxins in soil, air and food.
The first evidence that dioxin may cause cancer was an animal study published in 1978 but it was not till 1997 that dioxin was classified as a human carcinogen (cancer causing agent) by the International Agency for Research on Cancer (IARC).
In animal models TCDD appears to be a strong promoter (helps it along) and weak initiator (starter) of carcinogenesis (development of cancer). It is therefore possible that a carcinogenic (development of cancer) response to TCDD exposure in humans depends upon exposure to other initiators such as cigarette smoking.
The Institute of Medicine (IOM) of the National Academy of Sciences in the United States of America carries out regular reviews on all the evidence (animal and human) to create a list of conditions that are accepted as being associated (at high levels) with exposure to TCDD.
The conditions that have been accepted in the sufficient evidence of health effects category by the Institute of Medicine, are Hodgkins disease, non-Hodgkins lymphoma, soft tissue sarcoma, chronic lymphocytic leukaemia and chloracne.
There is limited or suggestive evidence that exposure to dioxins may help to cause respiratory cancers (lung, larynx and trachea), prostate cancer, multiple myeloma, acute and sub-acute transient peripheral neuropathy, porphyria cutanea tarda, Type II diabetes, and spina bifida in off-spring.
6. Where was dioxin produced in New Plymouth?
The former Ivon Watkins-Dow (IWD), now Dow AgroSciences (NZ) Ltd, chemical plant located in Paritutu, New Plymouth, manufactured the herbicide
2,4,5-trichlorophenoxyacetic acid (2,4,5-T) from 1962 to 1987. Trichlorophenol (TCP), which is an intermediate in 2,4,5-T manufacture, was manufactured on site from 1969. During TCP manufacture, dioxin (TCDD) is formed and remains as a contaminant in 2,4,5-T. Production of 2,4,5-T ceased in 1987.
2,4,5-T was used extensively throughout New Zealand to control gorse.
7. The serum dioxin study in Paritutu.
In October 2001 the Ministry of Health contracted the Institute of Environmental Science and Research Ltd (ESR) to investigate non-occupational exposure to dioxins among current and former Paritutu residents. Community consultation occurred between October 2001 and May 2002 resulting in agreement from the majority that blood serum testing was the appropriate mechanism for assessing this exposure. The report of this first phase was peer reviewed prior to its public release in March 2003.
A study protocol was then prepared for the next phase of the study and ethical approval obtained in May 2003 from the Taranaki Regional Ethics Committee.
8. How were the participants selected in the serum dioxin study?
Advertisements were placed in the national and local media asking for people who had lived in Paritutu for more than one year in the 1960s and 1970s to be a part of this study. To be included in the study, participants needed to have lived within a two kilometre radius east and one kilometre south of the former Ivon Watkins Dow plant for at least one year between 1962 and 1975, and have no history of exposure in their working life to dioxins or significant period of residence outside New Zealand.
The period from 1962 to 1975 was assumed to be the period of peak exposure based on:
* air emissions data from the incinerator stacks from 1975 on,
* 2,4,5-T production volumes, and
* the level of TCDD in 2,4,5-T.
In this phase of the study a potentially highly exposed group of current and former residents were then identified from a self-selected sample of the
population based on spatial (where they lived in relation to the plant), toxicokinetic (the way dioxin works in the body of different age groups and both sexes) and multi-pathway exposure (different ways people may have been exposed) modelling.
The exposure model considered the place, and years of, residence in relation to what was assumed to be the peak time period of any possible exposure (1962-1975). From this, people mostly likely to have been highly exposed were selected for serum testing.
Blood was taken from 24 participants in February 2004 and the results were compared with those obtained in a national serum study carried out by the Ministry for the Environment (MfE) in 1996-7. Blood is yet to be taken from about 20 people who have completed the study questionnaires and have been identified as potentially highly exposed.
9. What did the serum dioxin interim report show?
This is the interim report of part one of the second phase of this study. Part two of phase two is yet to be completed. Phase one was completed in March 2003. The phase one report is on the Ministry’s website along with this interim report of phase two.
In this report, ESR concluded that there was a statistically significant elevation in serum TCDD compared to national TCDD serum concentrations in the
study group. The mean serum TCDD level for the group was 10.8 pg/g lipid, with a range of between 1.3 to 33.3 pg/g, while the expected national mean for a similar group was 3.5 pg/g lipid.
Duration of residence in the area (within 1000m to the east and about 400m to the south) was important in determining the likelihood of an individual having an increased TCDD level.
Residents who had lived in Paritutu for more than 20 years between 1962 and 1987 in that defined area were more likely to have an elevated TCDD level.
Consumption of home-grown produce, including home grown poultry and eggs, did not appear to contribute significantly to elevations in TCDD.
The ESR report concluded that the findings supported the premise that aerial emissions containing TCDD were responsible for the soil and serum dioxin
concentrations in Paritutu. Whether these emissions were a result of regular or more episodic releases could not be determined by the current study.
10. The findings ESR reported were:
Elevations in serum dioxin (TCDD) reflect primarily duration of residence over the period 1962-1987 in areas of modelled soil TCDD in excess of 3.4pg/g.
These elevations are in all probability due to inhalational exposure from aerial emissions originating from the IWD plant.
The areas from which people were tested forms a narrow band around the perimeter of the Dow Agrosciences (NZ) Ltd plant, including approximately 500
11. The report stated the following questions remain unanswered:
* The timing of exposure in the period 1962 to 1987
* Peak dioxin levels in the sample group
* Serum TCDD levels in individuals who resided in areas where soil TCDD exceeded those in the study
* Whether there was a contribution to TCDD exposure from production of chlorinated phenolic products other than 2,4,5-T.
* Characterising the risk to the health of people significantly exposed
* Characterising the exposure of residents not included in this study.
12. So how did these people with elevated levels get exposed?
The report from ESR states that the: “elevations are in all probability due to inhalational exposures from aerial emissions originating from the IWD
13. What does this mean for those people?
Some people in the Paritutu community have in the past been exposed to TCDD at significantly higher levels than the typical New Zealand population.
It is possible that the TCDD levels found may have adverse health consequences for individuals or may cause increased rates of disease, in particular
cancer, on a population basis. The extent of the cancer risk is highly uncertain but based on the evidence to date from more highly exposed groups it
is estimated that it may be up to be 10 per cent above the national cancer mortality rate. [Refer Q19 for more detail.]
One in three deaths among the New Zealand population every year are from cancer. The major risk factors for cancer in New Zealand are cigarette smoking and poor diet. Lung cancer and colorectal cancer each cause more than 1000 deaths per year. Risk factors have been estimated for around 21,000 of the 26,000 deaths in New Zealand each year. Of these, it is estimated that 8500 deaths are due to poor diet, 5000 to tobacco, 800 to
alcohol, and 500 to road traffic injuries (Looking Upstream: Causes of death cross-classified by risk and condition, based on 1997 figures).
However, from studies that have been done on the New Plymouth community to date, (cancers and birth defects) there is no indication of increased disease rates in this population attributable to dioxins. However data limitations with this work mean the possibility of a small increased risk cannot be excluded.
14. What is the comparison with other international studies?
The blood TCDD levels estimated at the last time of exposure from three occupational cohorts are 2000pg/g (mean) up to 32,000pg/g, 1000 to 2400pg/g, and 345-3890pg/g. These groups have shown an increased mortality (death rate) from all cancers combined.
A study of nine New Zealand 2,4,5-T applicators, with an average of 193 months spraying, found the average TCDD serum level (53.3 pg/g lipid) in 1988 was almost 10 times that for the matched control subjects (average 5.6 pg/g lipid). In general, the serum TCDD level increased with total duration of 2,4,5-T exposure. These applicators had sprayed 2,4,5-T for a range of 83 to 372 months and given the half-life of TCDD, the findings suggest that the increase in TCDD would be about 3 pg/g among workers who only sprayed for one year. The half life is the time estimated for the body to excrete half of the dioxin it contains (estimated to be 7-10 years).
These data may not be representative of the general population of these geographical areas.
Country, TCDD (Pg/g lipid):
Seveso, Italy (non-exposed), 4.9
South Vietnam, 3.4 – 28
North Vietnam (Hanoi), < 2.4
In some geographical areas other dioxins are a much greater contributor to total toxicity than TCDD e.g. toxic equivalents for all dioxins for Germany are similar to USA and two areas (Binh Hoa, Dong Nai) in South Vietnam despite lower TCDD levels.
Following the Seveso (Italy) industrial incident in 1976 three exposure zones were classified based on decreasing soil TCDD levels. Populations of the
zones at the time of the incident were about 730 (highest exposure), about 5,900 (mid-range zone of exposure) and about 38,000 (low exposure). About
232,000 people from the surrounding non-exposed area have been followed up to serve as the reference population.
In 1996 (20 years later) the average TCDD results among randomly sampled exposed residents were 53.2pg/g for those in the highest exposed zone and 11pg/g in the mid-range exposed zone. This compares to 4.9pg/g in the non-exposed zone. This study excluded people with severe medical illness and previous chloracne.
The mean Paritutu serum TCDD result of 11pg/g is similar to some, but not as high as the highest, reported results found in areas of central and south Vietnam where aerial spraying of Agent Orange is known to have occurred about 20-28 years previously. It is the same as the mid-range exposed zone of Seveso, 20 years after the incident.
15. Should I get my blood tested if I lived in Paritutu?
Individual blood dioxin testing is not recommended. Tests for measuring dioxin levels in people are not routinely available and cannot be used to predict whether health effects will develop or not. There are only a few laboratories in the world who are accredited by the World Health Organisation as being able to detect these small amounts of dioxin in serum. These tests are costly and require a large amount of blood to be taken.
16. Is it safe to live in Paritutu now?
There is presently no greater risk for people living in Paritutu now than any other part of New Zealand that authorities are aware of.
A 2002 study of residential soil in the Paritutu area by the Ministry for the Environment found TCDD at all sites investigated, but all but one (from a grassed reserve on Mount Moturoa) result were below the most conservative international residential guidelines set to protect people’s health. The low levels measured mean that any risk to health of current and future residents from dioxin present in residential soil is negligible.
These soil findings are consistent with historical emissions from the plant as the source of TCDD in the area. The level of TCDD is normally low in relation to other dioxins when the primary source of dioxin is combustion. A previous MfE study, which was published in 1998, did not find TCDD in urban soils in any parts of the country other than New Plymouth.
The ESR interim report said concentrations tend to be highest close to the former IWD plant, and drop off rapidly within 800 to 1000 metres from the plant. Concentrations to the east of the plant, towards Mount Moturoa Domain, are higher than to the south of the plant. This is consistent with the prevailing winds in the area.
ESR concluded that consumption of home-grown produce, including home grown poultry and eggs, did not appear to contribute to elevations in TCDD.
17. How can I reduce my dioxin exposure?
Everyone has some dioxins in their body although levels in the general population are decreasing. Reduction in the amount of animal fat in the diet reduces dioxin exposure although it is not recommended that all fat be eliminated from the diet as a moderate amount is part of a healthy balanced diet. Not smoking and not burning rubbish, particularly plastics or driftwood, all help to reduce individual exposures.
18. Does New Plymouth have a high rate of birth defects?
In 2002, the Medical Officer of Health for New Plymouth, Dr Patrick O’Connor conducted a study into the rate of birth defects notifications in New
Plymouth. He found a lower rate of birth defects notifications (1988-99) compared to the New Zealand population.
The New Plymouth rate of neural tube defects (1965 -72) was slightly higher than the estimated national rate but the difference was not statistically significant. Three cases were identified from an area near IWD, which is two cases more than what was expected based on the New Plymouth rate.
Although not a statistically significant difference there are uncertainties with the data. Neural tube defects include spina bifida and anencephaly.
19. Does New Plymouth have higher rates of cancer?
Dr Patrick O’Connor, Medical Officer of Health, has carried out a study in response to public concerns about health effects associated with living near the former IWD plant. No difference in cancer registrations (1990-97), and six per cent (within the range of variation expected by chance) higher cancer mortality (1988-97) was found compared to the New Zealand population. The results do not exclude a small increased cancer risk.
To date there is no clear indication of increased disease rates in the population attributable to dioxins. Current data limitations such as the small
size of the population mean the possibility of a small increased risk cannot be excluded.
It is possible that the TCDD levels found may have adverse health consequences for individuals or may lead to increased rates of disease, in particular cancer, on a population basis. The extent of the cancer risk is highly uncertain but based on the evidence to date from the more highly exposed IARC occupational cohort and the Seveso cohort it is estimated that it may be up to 10 per cent above the national cancer mortality (death) rate.
If there were 100 people who lived in the highly exposed area of Paritutu for more than 20 years between 1962 to 1987, they might have up to a 10 per cent
increase in their risk of dying from cancer, above their existing risk (which is 33 per cent). This means that of those 100 people:
* there would be 3 deaths or less from dioxin exposure
* 3.5 would die from air pollution
* 18 would die from cancers due to tobacco smoking
* 3 from alcohol consumption
* 29 from poor diet.
A cancer mortality atlas published in 1982 by the Department of Health using 1974-78 mortality data found a higher rate of non-Hodgkin’s lymphoma and Hodgkin’s disease in New Plymouth compared to the national average. At that time there was no scientific evidence of an association between lymphatic cancer and dioxin. These two cancers are included in a study of cancer rates in New Plymouth currently being undertaken.
20. What if I have some of the symptoms of these diseases or I am concerned about my health?
You should contact your local Medical Officer of Health and discuss with him, or her, your concerns. The Medical Officer of Health will meet with you if you wish. In addition, all General Practitioners in New Plymouth and throughout New Zealand have been provided with information about this study and the known effects of dioxin.
21. What will happen now?
This study is only part way through, a second stage of further testing is be carried out by ESR. The Ministry is waiting for this further work to be completed. It is hoped that this further work will provide some answers to those questions that remain unanswered.
22. What has been done to investigate the concerns of this community?
Following community concern after a bursting disc failure at the plant in April 1986, the Minister of Health directed an Inquiry to be conducted. It found no substantiated evidence that 2,4,5-T manufacture had any adverse effect on residents’ health (Brinkman report 1986). It wasn’t till 1997 that TCDD was classified by the International Agency for Research on Cancer (IARC) as a human carcinogen.
In 2001, a group of government Ministers met and decided to implement an all-of-government approach to organochlorines (of which dioxin is one) issues in New Zealand because of the public concerns that had been raised.
The Ministry of Health was tasked with co-ordinating this group, which includes the Ministry for the Environment, ACC, the Department of Labour, the
Ministry of Agriculture and Forestry, the New Zealand Food Safety Authority and Veterans Affairs.
In September 2001, the Taranaki Regional Council released their report on alleged historical dumpsites used by the former IWD. No evidence of inappropriate disposal was found at any of the 36 separate sites investigated.
Also in September 2001, officials from the Ministry of Health and the Ministry for the Environment met with members of the Taranaki Regional Council, the New Plymouth District Council, the Taranaki District Health Board and its public health unit. It was agreed by all parties to take a coordinated approach to soil and blood testing.
In August 2001, Dr Patrick O’Connor, Medical Officer of Health for Taranaki, carried out a study in response to public concerns about health effects associated with living near the former IWD plant. No difference in cancer registrations (1990-97), and six per cent (within the range of variation expected by chance) higher cancer mortality (1988-97) was found compared to the New Zealand population. The results do not exclude a small increased cancer risk.
In August 2002, Dr Patrick O’Connor released a report on birth defects data for 1965 – 1971 in response to concerns raised by data collected by a former nurse from Westown Maternity Hospital, New Plymouth. The rate of neural tube defects (spina bifida and anencephaly) was slightly higher than the estimated national rate but the difference is not statistically significant. Three cases were identified from an area near IWD – although this is two cases more than what was expected based on the New Plymouth rate the finding is of uncertain statistical significance because of problems with the data and definition of the study area.
23. What studies are currently underway for this community?
The Ministry of Health is also conducting a study of certain cancer incidence and mortality in New Plymouth. The cancers under study are soft tissue sarcoma, non-Hodgkin’s lymphoma, Hodgkin’s disease and chronic lymphocytic leukaemia. These cancers have been associated with exposure to herbicides such as 2-4-5T.
24. Are health agencies able to quickly diagnose the health effects that have been associated with dioxin?
The cancers that have been found to be linked with high levels of dioxin exposure are very rare and are generally treatable if identified early.
25. If my dioxin levels are elevated should I go to even greater lengths to limit my exposure in future?
Previous studies of the New Zealand population show that dioxin levels have dropped by as much as 70 per cent in the last ten years and this will continue to decline. It is estimated that 90 per cent of New Zealanders exposure comes through the food chain and as emissions to the environment decline New Zealanders exposure will continue to be reduced.
New Zealand is one of 50 countries to sign the Persistant Organo-pollutants (POPs) Treaty, in 2001, and this involves the reduction and elimination of
26. What are the Ministry of Health and local health services doing to treat me?
There is no treatment for removing dioxin in the body. The body naturally excretes half of the dioxin it holds every 7 to 10 years and as dioxin emissions to the environment are declining it will continue to reduce in our bodies.
But now that we are aware of this elevated level in some members of this community, the health system can ensure that this is taken into account in their general health care.
27. What do I do if this study has raised concerns for me?
Your local Medical Officer of Health is available to discuss your concerns and will meet with you if you wish. In addition, all General Practitioners in New Plymouth and throughout New Zealand have been provided with information about this study and the known effects of dioxin.
28. What further investigation will there be?
This is only an interim report detailing the first partof a two phase study involving serum testing. The second part of this serum testing will be completed by the end of the year.
29. What is the Ministry of Health doing?
The Ministry of Health is:
* completing the Serum Dioxin Study
* conducting a study of certain cancer incidence and mortality in New Plymouth
* 0800 555 567 provides information and answers queries
* local Medical Officers of Health are available to discuss people’s concerns
* all General Practitioners have been provided with information
* personal follow-up for people who were tested as part of Part 1 of the study
* follow up with community groups about future actions
* coordination of a whole of Government response to organochlorines issues.
Sep 9, 2004 | nzherald.co.nz |