UNIVERSITATEA DE ŞTIINŢE

AGRICOLE ŞI MEDICINĂ VETERINARĂ

CLUJ-NAPOCA
FACULTATEA DE AGRICULTURĂ
MASTERAT:
Food Quality Management

Dioxins

Analysis of risks for DIOXINS

Îndrumator Masterand
Prof. dr. SOCACIU CARMEN SASU BIANCA

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Table of content

I. RISK ANALYSIS............................................................................................................3
Chemical risk assessment................................................................................................3
1.1.1 Description of hazard..........................................................................................3
1.1.2 Occurrence..........................................................................................................3
..............................................................................................................................................4
II. HAZARD CHARACTERIZATION...............................................................................4
Hazard identification.......................................................................................................4
2.1. Toxicity....................................................................................................................4
2.1.1 Toxicity in experimental animals .......................................................................5
2.1.2 Effects on Humans .............................................................................................7
2.1.3 Toxic Equivalent Factors ...................................................................................8
III. EXPOSURE EVALUATION .....................................................................................10
3.1. Analytical aspects ..................................................................................................10
3.2 Intake data ...............................................................................................................10
IV. EXPOSURE ASSESSMENT......................................................................................11
4.1. Sources of human exposure....................................................................................11
V. METHODS OF ANALYSIS........................................................................................12
VI. EXPOSURE ANALISYS............................................................................................14
VII. RISK MANAGEMENT AND RECOMMENDATIONS .........................................15
7.1 Recommendations for emission-reducing measures ..............................................15
7.2 Recommendations for risk management in foods ...................................................16

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I. RISK ANALYSIS

Chemical risk assessment

1.1.1 Description of hazard

Polychlorinated dibenzo-p-dioxins (PCDDs) and dibenzofurans (PCDFs) are halogenated
aromatics compounds that have been identified as contaminants in almost every
component of the global ecosystem including the air, aquatic and marine sediments, fish,
wildlife and human adipose tissue, milk and blood. PCDDs and PCDFs are industrial by-
products that are formed during the production of chlorinated phenols and their derived
products and other chlorinated compounds. These contaminants have also been identified
as by-products from the combustion of municipal and industrial waste, petrol, wood, coal
and numerous other combustion processes. Lastly, PCDDs and PCDFs are formed during
the bleaching of wood and pulp paper, and during metal-producing and metal-recycling
processes. The structures of individual PCDD and PCDF congeners differ by their degree
of chlorination and the ring substitution patterns. There are 135 individual PCDFs and 75
individual PCDDs. The composition of the PCDD and PCDF by-products are highly
variable dependent on their source. However, quantitative analysis of PCDDs/PCDFs in
environmental matrix requires a number of different procedures in order to prepare
concentrated and cleaned extracts before analysis by gas chromatography combined with
mass spectrometry technique. Such analysis is expensive and is a limiting factor for
monitoring programmes.

1.1.2 Occurrence
Dioxins occur as a complex mixture in the environment and in food. In
order to assess the potential risk of the whole mixture, the concept of
toxic equivalence has been applied to this group of contaminants.
TCDD, the most toxic member of the family, is used as reference
compound, and all other dioxins are assigned a toxic potency relative
to TCDD, based on experimental studies. During the last 15 years,
WHO, through the International Programme on Chemical Safety (IPCS),
has established and regularly re-evaluated toxic equivalency factors
(TEFs) for dioxins and related compounds through expert
consultations. WHO-TEF values have been established which apply to
humans, mammals, birds and fish. The last such consultation was held
in 2005 to update human and mammalian TEFs. These international
TEFs have been developed for application in risk assessment and
management, and have been adopted formally by a number of
countries and regional bodies, including Canada, Japan, the United
States and the European Union.

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II. HAZARD CHARACTERIZATION

Concern over dioxins arose initially because one particular congener, 2,3,7,8-TCDD, was
found to be extremely toxic to some types of laboratory animals. Toxic potency has been
demonstrated to be associated with the number and position of chlorine atoms, since
congeners lacking chlorines in the four lateral positions, as well as those having chlorines
in addition to those in the 2,3,7 and 8 positions, have been shown to be less toxic than
TCDD. In addition, congeners chlorinated in the lateral positions have been found to
accumulate preferentially in animal tissues and have been implicated in the human
poisoning incidents. As a result of toxic potency, widespread distribution, persistency and
potential for bioaccumulation of congener mixtures available for human exposure, dioxin
risk assessment requires a number of analytical, toxicological and epidemiological data.

Hazard identification

2.1. Toxicity
The toxicokinetic of PCDDs/PCDFs is related to their characteristics in terms of
lipophilicity and susceptibility to CYP dependent metabolism. Absorption of PCDDs and
PCDFs after oral administration is dependent on the vehicle used but remains very high
(ranging from 60 to 90%), both in experimental animals and humans. However,
elimination is much slower in man (T1/2 about 7 years for TCDD in man compared to a

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few weeks in rodents). Congeners with few chlorine atoms are usually metabolised and
eliminated faster than higher chlorinated ones. The body burden in animals and humans
can be easily estimated by measurements in tissues and plasma lipids.

2.1.1 Toxicity in experimental animals

The acute LD50 of TCDD varies over 5000-fold range between Guinea pig (most
sensitive) and Hamster. Among PCDDS and PCDFs, 2,3,7,8-TCDD exhibits the higher
toxic potency. Toxicological effects of PCDDs have been found dose-related and thus are
relevant to risk assessment for man:
1) induction of hepatic monooxygenases,
2) effects on components and functions of the immune system,
3) reproductive and developmental toxicity,
4) organ toxicity,
5) effects on hormone systems,
6) effects on the central nervous system
7) carcinogenicity.
For carcinogenicity, TCDD is regarded as a promotor and is not genotoxic. Therefore, a
classic approach via NOAEL and safety factors seems adequate for risk assessment.
Toxic dioxins may cause non-cancer effects to animals, affecting development,
reproduction, the immune system and the uterus. Human background exposures in
industrialized countries have sometimes reached levels at which these effects were seen
in animals.
In laboratory testing, TCDD and some other types of dioxins increase the number of
cancers in several animal species, in both sexes. They do not initiate cancers but promote
the growth of existing precancerous cell.
2,3,7,8-TCDD has been shown to be carcinogenic to multiple animal species of both
sexes. Most dioxins do not initiate cancer as such, but indirectly promote growth and
proliferation of previously initiated cancerous lesions.
The cancer observed at the lowest exposure are liver tumors in rats. 2,3,7,8-TCDD also
caused thyroid tumors in male rats.
Several other dioxin types have also been shown to be cancer promoters.

Carcinogenic effects

2,3,7,8-TCDD has been shown to be carcinogenic in several chronic studies at multiple

sites in multiple species in both sexes. Short-term studies observed a lack of direct DNA-
damaging effects including covalent binding to DNA by TCDD, which underscores that
TCDD is not acting as an initiator of carcinogenesis. However, secondary mechanisms
may be important in the observed carcinogenicity of TCDD and related dioxin-like
compounds.
The lowest observed adverse effect of TCDD in the Kociba study was the development of
hepatic adenomas in rats at an intake of 10 ng/kg bw/day and the no observed effect level
was 1 ng/kg/day. At the no observed effect level, body burdens were 60 ng TCDD/kg bw.

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 TCDD also causes thyroid tumours in male rats. This has been indicated to proceed
through a mechanism which involves altered thyroid hormone metabolism, and
consequent increases in feedback mechanisms (TSH) which results in a chronic
proliferative stimulation of thyroid follicular cells.
Studies in the mouse skin support a lack of initiating activity and an ability to promote
the growth of previously initiated lesions indicative of a promoting agent. Mouse skin
tumour promotion indicates that the Ah receptor is involved in tumour promotion by
TCDD. Extensive examination of liver tumour promotion in the female rat liver also
supports a non-genotoxic mechanism for the induction of liver neoplasms by TCDD. The
ability of TCDD to enhance proliferation and inhibit apoptotic processes in focal hepatic
lesions further supports an indirect mechanism of carcinogenicity.
Several PCDDs, PCDFs, non-ortho and mono-ortho PCBs have also been shown to be
tumour promoters.

MOST SENSITIVE EFFECTS OF 2,3,7,8-TCDD IN ANIMALS

Effect Species Exposure Maternal body burden

(LOEL or LOAEL) (increment to
background)*
Adverse effects
Developmental effects
- neurotoxicity (object Rhesus ~160 pg/kg/d 42 ng/kg**
learning) monkey
Reproductive toxicity rat
- decreased sperm count 64,000 pg/kg*** 28 ng/kg
- vaginal threads 200,000 pg/kg*** 73 ng/kg
Immunotoxicity rat 100,000 pg/kg*** 50 ng/kg
Immunological (viral mouse 10,000 pg/kg*** 10 ng/kg
sensitivity)
Hormonal Rhesus ~160 pg/kg/d 42 ng/kg**
(endometriosis)
monkey
Effects which may or may not lead to adverse effects
Biochemical effects
-CYP1A1 mouse 150 pg/kg/d 3 ng/kg
rat 100 pg/kg/d 3 ng/kg
-CYP1A2 mouse 450 pg/kg/d 10 ng/kg
-EGFR rat 100 pg/kg/d 3 ng/kg
-IL1beta mouse 300 pg/kg/d ~10 ng/kg
Functional effects
-oxidative stress mouse 450 pg/kg/d 10 ng/kg
-lymphocyte subsets marmoset ~200 pg/kg/d 6-8 ng/kg
monkey

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Tolerable Daily Intake (TDI)

European governments have developed a range of TDIs depending on the toxicological

endpoints observed and the safety factors applied at the endpoint. In 1990 the WHO
recommended a TDI of 10 pg I-TEQ/kg bw/day. This TDI was based on carcinogenic
effect in rat (NOAEL 10 ng I-TEQ/kg/day and safety factor of 1000) and on primate
reproductive performance (NOAEL of 1 ng I-TEQ/kg/day and safety factor of 100). The
UK and Belgium have adopted the WHO recommendation of 10 pg I-TEQ/kg/day.
Sweden, Norway and Finland have adopted a TDI of 5 pg I-TEQ/kg/day using a safety
factor of 200. The Netherlands adopted, in 1982, a TDI of 4 pg I-TEQ/kg/day with a
safety factor of 250 and recommended recently to reduce the TDI to 1 pg I-TEQ/kg/day.
In France, safety factors of 50-1000 have been applied to obtain TDIs in the range of 1-
10 pg I-TEQ/kg/day. In Germany, a similar range of TDIs was obtained using safety
factors of 100-1000, 1 pg I-TEQ/kg/day being regarded as a non-statutory precautionary
TDI, and 10 pg I-TEQ/kg/day as a preventive or intervention TDI. The American
Environmental Protection Agency (EPA) has proposed a virtual safe dose of 0.006
pg/kg/day, corresponding to an acceptable lifetime tumour risk of 10-6. In Japan, the TDI
was recently reduced to 5 pg I-TEQ/kg/day. In the light of current scientific knowledge, it
can be generally assumed that an exposure lower than 1 pg I-TEQ/kg/day does not
present adverse human health implications. The 1998 WHO-consultation recommended
that every effort should be made to reduce exposure to the lower end of the advised range
of 1-4 pg TEQ/kg bw/day.

2.1.2 Effects on Humans

Health effects such as chloracne have been identified as an effect of dioxins in humans.
Epidemiological data on dioxins have been collected through studies on victims of
accidents, occupational exposure and on veterans who were engaged in herbicide
scattering operations in the Vietnam war. Records

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of poisoning of humans by furans include cases of cooking oil contamination in Japan
and Taiwan.
In February 1997 the IARC classified 2,3,7,8-TCDD as a «known» human carcinogen,
but continues to regard other PCDDs/PCDFs as «not classifiable» despite a similar mode
of action to 2,3,7,8-TCDD. Other effects than carcinogenicity have been studied in
humans as discussed in a recent Toxicology Forum in Berlin (1996). The following acute
effects have been observed: chloracne, porphyria cutanea, liver dysfunctions, respiratory
and neurological disorders, increased diabetes susceptibility, and changes in lipids
parameters in blood. Recent epidemiological studies have focused on the anti-oestrogenic
effect and subtle developmental effects in infants and children. However, since
confounding factors may have been present, any or all of the effects observed cannot be
ascribed specifically to dioxine exposure.
Most of the comparisons between human and animal dioxin toxicity refer to the
mechanism of action based on binding to Ah receptor. Activation of the Ah receptor can
result in endocrine and paracrine disturbances and alterations in cell functions, including
growth and differentiation. Some of these effects have been observed both in humans and
animals, indicating the existence of common mechanisms of action. However, the human
Ah receptor has a lower affinity for TCDD binding than rodents, suggesting that humans
may be one order of magnitude less sensitive to TCDD than mice and rats. It has been
demonstrated that the induction of CYPIA1 in human lymphocytes by TCDD falls into a
bimodal distribution with high responders and low responders. A high inducibility
phenotype for CYPIA1 induction may be associated with increased susceptibility to lung
cancer. Moreover, Ah receptor mediated CYP1A induction can be obtained without
ligand binding. These points are very important for the choice of safety factor in TDI
calculation.

2.1.3 Toxic Equivalent Factors

Although there are extensive data on the toxicity of 2,3,7,8-TCDD, toxicological
information on the other 209 compounds in the family is much more sparse. In order to
help in the toxicological evaluation of complex mixtures, a concept of toxic equivalent
factors (TEFs) has been developed, taking in account the mechanism of action of PCDDs
and PCDFs. Although 2,3,7,8- TCDD is the most potent congener able to bind Ah
receptor, other compounds that interact with this receptor result in similar effects, albeit
at higher doses. These relative potencies are expressed as TEFs. After examining the
relative potency of different PCDDs and PCDFs for a variety of end points both in vitro
and in vivo, such as cancer, reproductive effects, body weight loss, cell transformation,
immunotoxicity and Ah receptor binding, a set of TEFs has been developed. In 1988 a
NATO/CCMS sub-committee proposed a new set called International TEFs adopted by
several regulatory agencies in North America and Europe. The TEF models contain many
sources of uncertainties related to a lack of scientific data on congeners, differences in
toxicokinetics and metabolism, the interaction between congeners, and to variations
between species and individuals. TEF values for human beings and mammals were
revised by the WHO in 1997. At the present time, the TEFs can be regarded as an interim
procedure to beimproved.

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Acute Toxicity

Characteristic feature of acute dioxin poisoning is the acne (Chloracne) - which was
widely publicized during the election of Viktor Yushchenko as president of Ukraine, and
altered liver tests exploration. Eruption disappeared gradually as the concentration of
PCBs in the blood decrease.
It is considered that intoxication in humans is over 95% of cases by food by dioxin in
meat consumption, especially animal fat, but also eggs, milk or other common foods. We
found a direct relationship between the amount of dioxin in the human body in a
community, and level of contamination of food and the environment in which ive. In the
U.S., it is believed that dioxin is found in highest concentrations in beef, and milk,
chicken, pork, fish, eggs, inhalation, soil and water lowest concentration.
Besides food, human contamination can be done by water, soil, inhalation of
contaminated dust, cigarette smoke, or absorption through the skin and the baby through
mother's milk.

Chronic Toxicity

Common chronic poisoning can have a much larger effect than acute, although they are
less obvious, the most commonly affected are the endocrine system and the reproductive.

Effects of chronic poisoning with dioxin on the human body

Leather - Hyperpigmentation, Chloracne

Endocrine - Type II diabetes, hypothyroidism
Reproduction - Endometriosis, decreased fertility, spontaneous abortions, testicular
atrophy, hypospermia, lower level testesteron
Gastrointestinal Abdominal pain, nausea, vomiting, weight loss, liver function tests
change, spleen damage
Immunological-Depression immune defense with an increased risk of infection
MetabolicThe increase of blood lipids, atherosclerosis
Children-Increasing delay, learning difficulty, adjustment problems, poor development
of teeth
Carcinogenic-Different types of cancers - breast, uterus, testis, prostate, skin
General-Muscle atrophy, fatigue.
Not all of these side effects are equally common. Tracking over the years the population
of the area Soveso intoxicated, showed an increasing number of cancers by about 10%,
but other possible effects have not been fully confirmed.
Although most intestinal dioxin profile data are those related to contamination of
different foods (especially meat), dioxin poisoning by this route is unlikely because low
doses of dioxin in meat. Chronic poisoning linked to contaminated meat consumption
only is possible only in conditions where an area to supply meat is made from a single
source and it can be contaminated, a situation unusual in a market economy as the Wider
Europe.

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III. EXPOSURE EVALUATION
3.1. Analytical aspects
Over the past three decades the analytical technology involved in the determination of
chlorinated PCDDs and PCDFs has evolved following advances in the science of both
isolating the analyses as well as identifying and measuring them. In the course of this
evolution, the techniques of mass spectrometry have been the primary driving force.
However, analytical methodology for dioxin samples from the environment and
foodstuffs remain difficult and costly, limiting the quantity and significance of the data
available.
PCDDs and PCDFs have been identified in extracts of samples from the environment and
the composition of these analyses depend on their origins and inputs from nearby sources.
The congener distribution for most atmospheric samples resembles the typical
combustion pattern for these compounds. Octa and hepta-CDDs are dominant in PCDD
profiles, and tetra and penta-CDFs are dominant among PCDFs. Similar patterns have
been detected in plant extracts. In contrast, only 2,3,7,8 substituted PCDDs and PCDFs
are currently detected in animal samples, while OCDD often remains the dominant
congener. In 1990, municipal incinerators appeared to be the major source of dioxins in
the atmosphere (from 47% in Germany to 82% in the Netherlands). In the past decades,
the manufacture of polychlorinated aromatic chemicals has probably been the major
source. Maximum air emission from combustion sources was evaluated from 926 g I-
TEQ/year in West Germany (1990) to 3870 g I-TEQ/year in the U.K. (1989). Dioxins
and furans are almost insoluble in water and therefore strongly adsorbed to soil and
organic matter where they persist for many years due to their chemical stability and
resistance to biodegradation. These compounds are thus available for biological
absorption, and first of all for organisms containing significant amounts of fat. Therefore,
PCDDs and PCDFs can contaminate food destined to human consumption and they are
more likely to be present in fatty foods such as meat, fish and dairy products, rather than
fruit, vegetables and drinking water.

3.2 Intake data

Human exposure to PCDDs and PCDFs is possible by several routes. Intake by inhalation
and by ingestion of contaminated particles is minor compared to the contribution from
contaminated foodstuffs. The data used here for food intake calculations are from various
surveys carried out by official bodies from different countries. The majority of the studies
has been conducted on cow’s milk and dairy products, fish and meat products. Other
foodstuffs investigated in some countries yield the relative contributions of major food
types for the estimation of the total dietary intake of dioxins and furans. The major route
of food contamination seems to be the ingestion of contaminated herbage (with any
adhering soil) and feed by cattle leading to the contamination of milk, meat and
derivative products. The concentrations in milk and dairy products range from 0.4 to 27
pg I-TEQ/g fat. The mean level of contamination in milk from retail samples is situated
between 0.4 and 2 pg I-TEQ/g fat. The mean content in samples from contaminated farms

10
ranges from 3 to 27 pg TEQ/g fat. PCDD and PCDF intake from milk and dairy products
is between 25 and 45% of the total intake. Similarly, meat and meat products (including
eggs and fat) provide nearly 25% of the total intake. Fish has been reported in the
literature to be a major dietary source of dioxins and furans for the populations around
the Baltic (up to 60%). As indicated previously, PCDD and PCDF contents in vegetables,
cereals and fruit are very low as can be expected for non-fatty foodstuffs. However,
cereal products containing significant quantities of added fat may contain appreciable
levels of PCDDs and PCDFs. Thus the contribution of vegetables is nearly 5% to the total
intake, while in countries which usually consume significant quantities of biscuits and
cakes cereal products can contribute up to 15% of the total intake. Thus the total intake in
European countries is in the range of 70 to 350 pg I-TEQ/person/day. A total diet study in
the UK reported a mean estimated dietary intake of 125 pg I-TEQ/day, and a calculation
from the Netherlands showed that the 99 percentile of the adult population had a dioxin
intake below 150 pg TEQ/day. Based on the intake data available from European
countries, it can be estimated that the intake of PCDDs/PCDFs in pg I-TEQ/kg/day
ranges from 1 to 5 for adults (70 kg) and from 3 to 12 for infants (13 kg).
Levels of PCDDs and PCDFs in human milk have been reported from different countries.
In Europe, the values range from 9 to 67 pg I-TEQ/g fat. Accordingly, the intake of
PCDDs and PCDFs by breast-fed infants has been estimated to vary from 27 to 418 pg I-
TEQ/kg /day.

IV. EXPOSURE ASSESSMENT

4.1. Sources of human exposure

Humans are exposed to dioxins and/or PCBs through either:
• accidental exposure,
• occupational exposure, or
• environmental exposure.

In the last few decades, several accidents have caused extensive exposure of humans to

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dioxins and dioxin-related compounds. Well-known examples are the exposure of the
local population at Seveso (Pocchiari et al., 1979; Bertazzi and di Domenico, 1994), and
from fires in PCB-filled electrical equipment, such as in the Binghamton State Office
Building (Fitzgerald et al., 1986, 1989). High exposures, with toxicity, may be caused by
the ingestion of accidentally contaminated food items. Known examples are the
contamination of edible oils, such as the Yusho (Japan) and Yu-Cheng (Taiwan) food
poisoning episodes (Rogan et al., 1988; Kuratsune et al., 1996).
Occupational activities in which TCDD and related compounds are unintentionally
produced, such as waste incineration or production of certain pesticides or chemicals,
may also result in a significant human exposure.
While accidental and occupational dioxin exposure is normally limited to more or less
small subgroups of the population, environmental exposure due to diffuse sources affects
allhumans. This exposure is possible by several routes:
• food consumption,
• inhalation of air and ingestion of particles from air,
• ingestion of contaminated soil,
• dermal absorption.
While the last three routes normally contribute less than 10% to the total daily dioxin
intake,
more than 90% of human dioxin exposure derives from food. Of this, about 90%
normally comes from foods of animal origin (Fürst et al., 1992). Contamination of food
is primarily caused by release of dioxins from various sources (e.g., waste incineration,
production of chemicals, metal industry), and their subsequent accumulation in the food
chain where they are particularly associated with fat. Other sources may include
contaminated feed, as occurred in Belgium in 1999 (Ashraf, 1999; Broeckaert and
Bernard, 2000), application of sewage sludge to farm land, flooding of pastures, waste
effluents, and certain types of food processing and preparation.
For most people, about 90% of overall exposure to dioxins comes
through diet. The Joint Expert Committee on Food Additives, an expert
group of the World Health Organization and the Food and Agriculture
Organization of the United Nations, has set a "tolerable monthly
intake" level for dioxins, furans and similar substances.
The "tolerable" level (meaning no serious health effects are expected)
is 70 picograms per kilogram of body weight / month. This is roughly
2.3 picograms per kilogram of body weight / day. A picogram is one-
trillionth of a gram.

V. METHODS OF ANALYSIS

The method of choice for the combined confirmation of dioxins is gas chromatography –
high resolutionmass spectrometry (GC/HR-MS) after extensive sample clean-up. This
expensive and time-consuming technique is only applied by a relatively small number of
laboratories. Thus, there will be a delay of several days between an incident and the
results of the analysis.

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Dioxin-like PCBs can also be determined by gas chromatography with other low-
resolution mass spectrometry instruments. For screening purposes of mixtures of dioxins
including dioxin-like PCBs, less expensive and more rapid bio-assays such as the Calux-
assay are applied. Although these bio-assays are successfully applied in various
laboratories, there is still a need for improvement with regards to robustness and
selectivity, although knowledge of the degree toxic effects of the mixture, which is
measured by thebioassay, is an important tool for risk management measures.
As analyses for dioxins by GCMS are quite expensive in comparison to determination of
other chemical contaminants, periodic tests should be performed to the extent feasible at
least by industrial feed and food manufacturers including both incoming raw materials
and final products and data should be kept. The frequency of sampling should consider
results from previous analysis (by individual companies and/or via a pool of industry
results within the same sector).

• Eggs are characterised by a rather recurrent PCDD and PCDF presence, with a mean
around 1 pg I-TEQ/g, lipid basis, and only a slightly higher value of the upper confidence
limit.
• Wild fish and freshwater fish from farms exhibit indistinguishable contamination levels,
on average centered around 10 pg I-TEQ/g, lipid basis, for dioxins and 30 pg PCB-
TEQ/g, lipid basis, for dioxin-like PCBs: the threefold difference of the means appears to
reflect a consistently higher contamination from PCBs, also confirmed by the
corresponding upper confidence limits. In spite of the small spreads exhibited by the CIs,
the recorded contamination ranges in fish span over two (for dioxin-like PCBs) to three
(for dioxins) orders of magnitude.
• Poultry, beef and veal, and mixed meat have similar concentrations of PCDDs and
PCDFs. The estimated <X> and CIs for pork meat are approximately half of those
reported for the other three subgroups; however, this difference is not statistically
significant. Game meat and liver have concentrations of PCDDs and PCDFs significantly
higher than the other meat subgroups. If the Meat and meat products group is
conservatively taken as a whole, this yields CI estimates for PCDDs and PCDFs and
dioxin-like PCBs spanning, respectively, the approximate intervals of 0.4-0.7 pg I-TEQ/g
and 0.3-1.5 pg PCB-TEQ/g, both on the lipid basis.
• Lastly, the subgroups of milk (“milk as such”) and its products (“others”) are
characterised by mean contamination levels within a factor of 2 for both groups of
analytes (approximately ranging from 0.6 to 1.0 pg I-TEQ/g or 0.6 to 1.3 pg PCB-TEQ/g,
lipid basis); however, differences are not significant. The upper confidence limits are in
the order of 1 pg I-TEQ/g, lipid basis, for PCDDs and PCDFs and fall in the approximate
range of 2-10 pg PCB-TEQ/g, lipid basis, for dioxin-like PCBs. The contamination
values reported for milk were obtained by excluding data associated with “industrial”-
type samples.

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VI. EXPOSURE ANALISYS

Many countries monitor their food supply for dioxins. This has led to early detection of
contamination and has often prevented impact on a larger scale. One example is the
detection of increased dioxin levels in milk in 2004 in the Netherlands, traced to a clay
used in the production of the animal feed. In another incident, elevated dioxin levels were
detected in animal feed in the Netherlands in 2006 and the source was identified as
contaminated fat used in the production of the feed.
Some dioxin contamination events have been more significant, with broader implications
in many countries.

In late 2008, Ireland recalled many tons of pork meat and pork products when up to 200
times more dioxins than the safe limit were detected in samples of pork. This finding led
to one of the largest food recalls related to a chemical contamination. Risk assessments
performed by Ireland indicated no public health concern. The contamination was traced
back to contaminated feed.

In July 2007, the European Commission issued a health warning to its Member States
after high levels of dioxins were detected in a food additive - guar gum - used as
thickener in small quantities in meat, dairy, dessert or delicatessen products. The source
was traced to guar gum from India that was contaminated with pentachlorophenol (PCP),
a pesticide no longer in use. PCP contains dioxins as contamination.

In 1999, high levels of dioxins were found in poultry and eggs from Belgium.
Subsequently, dioxin-contaminated animal-based food (poultry, eggs, pork), were
detected in several other countries. The cause was traced to animal feed contaminated
with illegally disposed PCB-based waste industrial oil.

In March 1998, high levels of dioxins in milk sold in Germany were traced to citrus pulp
pellets used as animal feed exported from Brazil. The investigation resulted in a ban on
all citrus pulp imports to the EU from Brazil.

Another case of dioxin contamination of food occurred in the United States of America in
1997. Chickens, eggs, and catfish were contaminated with dioxins when a tainted
ingredient (bentonite clay, sometimes called “ball clay”) was used in the manufacture of
animal feed. The contaminated clay was traced to a bentonite mine. As there was no
evidence that hazardous waste was buried at the mine, investigators speculate that the
source of dioxins may be natural, perhaps due to a prehistoric forest fire.

Large amounts of dioxins were released in a serious accident at a chemical factory in

Seveso, Italy, in 1976. A cloud of toxic chemicals, including 2,3,7,8-Tetrachlorodibenzo-
p-dioxin, or TCDD, was released into the air and eventually contaminated an area of 15
square kilometres where 37 000 people lived. Extensive studies in the affected population
are continuing to determine the long-term human health effects from this incident. These
investigations, however, are hampered by the lack of appropriate exposure assessments.
A minor increase in certain cancers and effects on reproduction have been detected and

14
are being further investigated. Possible effects on the children of exposed people are
currently being studied.

TCDD has also been extensively studied for health effects linked to its presence as a
contaminant in some batches of the herbicide Agent Orange, which was used as a
defoliant during the Vietnam War. A link to certain types of cancers and also to diabetes
is still being investigated.

Earlier incidents of food contamination have been reported in other parts of the world.
Although all countries can be affected, most contamination cases have been reported in
industrialized countries where adequate food contamination monitoring, greater
awareness of the hazard and better regulatory controls are available for the detection of
dioxin problems.

A few cases of intentional human poisoning have also been reported. The most notable
incident is the 2004 case of Viktor Yushchenko, President of the Ukraine, whose face
was disfigured by chloracne.

VII. RISK MANAGEMENT AND RECOMMENDATIONS

7.1 Recommendations for emission-reducing measures
The currently estimated food intake of TCDD equivalents by adults is lower than the
WHO TDI, but higher than the guideline level. Since PCDDs and PCDFs are known to
be persistent in the environment, their levels tend to increase as a result of continuous
release. Therefore, the introduction of these compounds into the environment should be
reduced. Accordingly, the following emission-reducing measures are recommended.
Incinerators: Emission of PCDDs and PCDs by all kinds of incinerators (including
municipal solid waste incinerators) should be limited to a maximum of 0.1 ng I-
TEQ/Nm3
Metal industry: Emission from metal-producing and metal-recycling industries should
be minimised by optimisation of technical procedures and equipment.
Motor vehicles: The use of halogenated scavengers in petrol should be phased out as
soon as possible.
Chlorine-containing chemicals: Production and use of chlorine-containing chemicals
such as certain pesticides and wood preservatives should be reduced in combination with
the reduction of the contamination of these products by dioxins and PCBs.
Pulp and paper industries: Bleaching processes other than involving chlorine treatment
should be adopted to minimise the presence of PCDDs and PCDFs in pulp and paper
products and effluent waste. For materials in contact with food the maximum level should
be reduced as much as possible.
Fireproofing substances: The use of PCB as fireproofing substances should be re-
examined
Other sources: Since the origin of a large fraction of PCDDs and PCDFs is not known,
every effort should be made to identify other sources of contamination pathways, in order
to take appropriate measures.

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7.2 Recommendations for risk management in foods
1) Emission-reducing measures are recommended as the best way for risk-management.
2) Main dietary intake of PCDDs and PCDFs is from milk and dairy products due to the
considerable consumption of these foodstuffs, particularly by children. Thus
standards in milk and dairy products should be recommended:
- Levels lower than 1 pg I-TEQ/g fat are a desirable target achievable after
reduction of PCDD pollution in the environment.
- Levels higher than 5 pg I-TEQ/g fat must lead to the consideration of a ban on
trade of affected milk and dairy products (fat content higher than 2%).
3) National and international monitoring of the levels of contamination in both milk and
dairy products as well as in fat from meat, fish, seafood and eggs is
recommended.
4) Monitoring of dioxins in human milk and blood is recommended as a way of obtaining
information on the level of human intake of these contaminants from foodstuffs.

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References:

http://www.hc-sc.gc.ca/hl-vs/iyh-vsv/environ/dioxin-eng.php

http://www.despreboli.ro/articole-medicale-noi-in-
rezumat/2008/12/intoxicatia-cu-dioxina/

http://www.clu-in.org/contaminantfocus/default.focus/sec/Dioxins/cat/Toxicology/

http://www.who.int/mediacentre/factsheets/fs225/en/index.html

http://cfpub.epa.gov/ncea/images/chaine.gif

http://www.google.ro/imgres?imgurl=http://www.sph.umich.edu/dioxin/images/fish
%2520advisory.JPG&imgrefurl=http://www.sph.umich.edu/dioxin

http://www.greenfacts.org/en/dioxins/index.htm

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