This article focuses on three types of food contaminants: dioxins including dibenzofurans and polychlorinated biphe-nyls, acrylamide, and perchlorate.. It is likely that concerns regardi
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Other Contaminants
C K Winter, University of California at Davis, Davis,
CA, USA
ª 2005 Elsevier Ltd All rights reserved.
Food may be contaminated with many chemicals
that pose the potential for toxicological
conse-quences in humans consuming the contaminated
food items In addition to the presence of
contami-nants such as mycotoxins, pesticide residues, and
heavy metals, food may contain numerous organic
contaminants that enter the food supply from
envir-onmental sources or as a result of chemical reactions
that occur during food processing This article
focuses on three types of food contaminants: dioxins
(including dibenzofurans and polychlorinated
biphe-nyls), acrylamide, and perchlorate Each of these
classes has been subject to considerable regulatory
scrutiny, scientific study, and popular media
cover-age It is likely that concerns regarding the presence
of these contaminants in the food supply will
con-tinue throughout the next decade or longer, and that
significant efforts will be made to reduce human
exposure to these substances from food This article
discusses how these types of food contaminants
enter the food supply, the types of food items in
which they are most likely to occur, and the
poten-tial toxicological consequences resulting from
expo-sure to these contaminants
Dioxins
Dioxins are organic chemicals that comprise a family of
ubiquitous environmental contaminants Technically
speaking, the dioxins of potential toxicological concern are polychlorinated dibenzo-p-dioxins (PCDDs) They are related, both structurally and toxicologically, to polychlorinated dibenzofurans (PCDFs) and poly-chlorinated biphenyls (PCBs) Structures of generic PCDDs, PCDFs, and PCBs are shown in Figure 1 Due to their structural and toxicological similarity and to avoid confusion, all three related groups of chemicals are considered to represent ‘‘dioxins’’ for the purposes of this article Specific chemicals belong-ing to this family are referred to as congeners Coll-ectively, there are more than 200 dioxin-related congeners, and each possesses unique toxicological and chemical properties
Occurrence in the Environment and in Food PCDDs and PCDFs are primarily introduced into the environment as by-products of combustion pro-cesses These by-products have been identified in the exhaust gases from sources such as cigarette smoke; industrial and municipal waste incinerators; power plants burning coal, oil, or wood; and automobiles
In addition to these human sources, PCDDs and PCDFs are also produced naturally by combustion
in forest fires and from volcanic eruptions
Historically, PCDDs and PCDFs have also been produced as impurities during organic chemical synth-esis The most notable and most toxic dioxin congener, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), has been shown to be produced in the synthesis of the herbicide 2,4,5-T, one of the herbicide components
of Agent Orange, notoriously used in the Vietnam War Although 2,4,5-T is now banned for use in the United States because of TCDD and other dioxin impurities, health concerns over the expo-sure of military veterans to Agent Orange and to TCDD continue to be raised PCDDs and PCDFs can also be produced through the use of chlorine
PCDD
O O
PCDF
O
PCB
Figure 1 Chemical structures of generic PCDDs, PCDFs, and PCBs.
Trang 2to bleach wood pulp, although most bleaching
processes now use nonchlorine agents such as
hydrogen peroxide
PCBs have been produced synthetically since the
1930s and have been widely used for industrial
applications, such as dielectric fluids in transformers
(due to their inflammability) and capacitors in
elec-trical machinery Like their PCDD and PCDF
coun-terparts, PCBs are extremely persistent in the
environment and are of toxicological concern As a
result, the synthesis and industrial use of PCBs were
significantly curtailed in the 1970s, although
envir-onmental residues of PCBs are still commonly
detected today
Although dioxin release into the environment has
been known to occur for several decades, data are
still limited with respect to the degree to which
dioxins contaminate the food supply Dioxin
analy-sis in the laboratory is extremely expensive because
methods must identify hundreds of different
conge-ners, detection limits are required in the sub-part per
trillion range, and significant precautions must be
taken to minimize exposure of laboratory personnel
to the analytical standards used for dioxin
congeners
Dioxins are highly fat soluble and have been
shown to accumulate in the fat of birds, fish, and
food animals The US Environmental Protection
Agency (EPA) has estimated that more than 95%
of human exposure to dioxins results from dietary
intake of animal fats The major food sources for
dioxin exposure include fish, poultry, meats, milk,
and milk products Dioxins are excreted in human
breast milk and result in exposures to nursing
infants
Historically, it has been shown that human dioxin
exposures, as determined by analyzing human
tis-sues and environmental samples, have decreased
sig-nificantly since 1987 due to engineering controls to
limit dioxin emissions during combustion processes
and to increased regulatory control over other
sources of dioxin exposure Dietary dioxin
expo-sures to UK consumers were reduced by nearly
two-thirds from 1982 to 1992, and subsequent
studies showed even lower exposures in 1997
Nevertheless, dioxins are still ubiquitous in the
environment and human exposure still occurs
Toxicological Considerations
Dioxin exposure at significant dose levels has been
linked to a large number of adverse health effects
Large acute exposures, resulting from chemical
acci-dents and/or occupational exposure to dioxins, have
caused a severe skin condition known as chloracne
A variety of other skin effects, such as rashes and discoloration, have also been attributed to acute dioxin exposures, as has liver damage
Concerns from chronic exposure to dioxins include cancer, reproductive effects, and develop-mental effects The most toxic dioxin congener, TCDD, was classified by the International Agency for Research on Cancer as a human carcinogen From a biochemical standpoint, PCDDs, PCDFs, and PCBs appear to cause their toxic effects through chemical binding to a specific cellular receptor known as the Ah receptor Specific dioxin congeners vary dramatically with respect to their abilities to bind with the Ah receptor; TCDD binds extremely effectively, whereas other congeners are more lim-ited in their binding capabilities The degree to which various dioxin congeners bind with the Ah receptor seems to be directly related to the number and location of chlorine atoms on the congeners Assessing the potential human health risks from exposure to dioxins presents significant challenges Dioxin levels in specific food items can be quite variable, and, as discussed previously, data concern-ing dioxin levels on foods are frequently not available
Another difficulty encountered in assessing dioxin risks is to appropriately account for exposures to the various congeners and to account for the toxico-logical differences among congeners This is most appropriately achieved through a toxic equivalency factor (TEF) approach that assigns a potency factor
to each of the congeners relative to that of the most toxic dioxin TCDD For example, the TEF for TCDD is 1 and the TEF for 1,2,3,4,7,8-hexachlor-odibenzo-p-dioxin (with chlorines added to the
1 and 2 positions and otherwise similar to TCDD) is 0.1 based on findings that 1,2,3,4,7,8-hexachlorodi-benzo-p-dioxin is 10 times less capable of binding to the Ah receptor than is TCDD To calculate a total dioxin exposure, the dietary contributions of each of the dioxin congeners are multiplied by their corre-sponding TEFs and summed to determine a TCDD equivalent exposure
According to the World Health Organization (WHO), a tolerable daily intake (TDI) for TCDD was established at 10 pg TCDD per kilogram body-weight per day in 1990, although revisions by WHO reduced the TDI range to 1–4 pg/kg/day in 1999 A
1997 UK survey of dioxin consumer exposure pro-vided an upper bound of 1.8 pg TCDD equivalent/ kg/day Surveys from other countries, using slightly different TEF approaches, yielded exposures of 0.7 pg/kg/day in Italy, 1.4 pg/kg/day in Norway, 2.4–3.5 pg/kg/day in Spain, and 0.2 pg/kg/day in New Zealand
FOOD SAFETY/Other Contaminants 341
Trang 3The US Food and Drug Administration (FDA) has
been monitoring finfish, shellfish, and dairy
pro-ducts for dioxins since 1995 and initiated dioxin
analysis of foods analyzed in its Total Diet Study
in 1999 Specific findings from the FDA’s annual
Total Diet Study can be obtained from the FDA,
although human exposure estimates, in terms of
the amount of TCDD equivalent exposure per
kilo-gram of body weight per day, have not been
pub-lished by the FDA
The EPA recommends that consumers follow the
existing Federal Dietary Guidelines to reduce fat
consumption and, subsequently, dioxin exposure
Such guidelines suggest that consumers choose fish,
lean meat, poultry, and low- or fat-free dairy
pro-ducts while increasing consumption of fruits,
vege-tables, and grains Dioxin exposure can be further
minimized by trimming visible fat from meats,
removing the skin of fish and poultry, reducing the
amount of butter or lard used in cooking, and
repla-cing cooking methods such as frying with methods
such as boiling or oven broiling
Acrylamide
Acrylamide is a widely used and versatile industrial
chemical Its most common use is as a coagulant in
water treatment and purification It is also used as a
soil conditioner, in the sizing of paper and textiles,
in ore processing, and as a construction aid for the
building of tunnels and dam foundations
Acrylamide is considered by the International
Agency for Research on Cancer to be ‘‘probably
carcinogenic to humans’’ based on the results of
several animal carcinogenicity studies As a result,
there has been widespread concern about the
poten-tial risks from exposure to acrylamide among
indus-trial, manufacturing, and laboratory workers
Consumer exposure to acrylamide in treated
drink-ing water has posed a much lower concern since
drinking water is subject to special treatment
tech-niques that control the amount of acrylamide in
drinking water
Swedish researchers developed laboratory
techni-ques that allowed for the detection of biological
reaction products (hemoglobin adducts) of
acryla-mide in human blood samples; results from their
studies allowed correlations to be made between
occupational activities and acrylamide exposures
The findings that acrylamide occurred in tobacco
smoke and that smokers had increased levels of
hemoglobin adducts relative to nonsmokers
pro-vided a suggestion that acrylamide may be formed
during incomplete combustion of organic matter or
during heating Interestingly, the researchers found
significant levels of hemoglobin adducts in blood samples of nonsmoking humans not exposed occupa-tionally to acrylamide This led to speculation that the human diet could contain significant quantities of acrylamide In April 2002, Swedish researchers pub-lished results of research that demonstrated the pre-sence of acrylamide in several common foodstuffs, with the highest levels found in fried and baked foods These findings stimulated worldwide interest
in identifying the potential mechanisms for acryl-amide formation in foods, in assaying a wide variety
of foods for acrylamide levels, and in developing risk assessment and risk mitigation procedures
Occurrence in Food The findings from the initial Swedish study indicated
that the highest levels (150–4000 mg/kg) of
acryla-mide were detected in carbohydrate-rich foods such
as potatoes and in heated commercial potato pro-ducts (potato chips) and crispbread Moderate levels
(5–50 mg/kg) were measured in protein-rich foods
that were heated, whereas unheated or boiled
foods showed no detectable acrylamide (<5 mg/kg).
The governments of several countries throughout the world performed similar analyses of acrylamide
in foods and findings were fairly consistent with those reported in the Swedish study The FDA ana-lyzed dozens of foods for acrylamide levels and con-cluded that the highest levels were observed in
french fries (29 samples; range, 117–1030 mg/kg)
117–2762 mg/kg) Multiple samples from different
lots of the same commercial food products showed significant variability, with the highest levels often several times greater than the lowest levels Com-mercial potato products that could be prepared by baking or by other methods showed much higher levels of acrylamide in the baked products Acryla-mide levels in baby food ranged from below the
detection level (<10 mg/kg) to 130 mg/kg All infant formula samples had levels below 10 mg/kg, and
acrylamide levels in dairy products were also low The widespread findings of acrylamide in food-stuffs throughout the world provided the basis for numerous studies designed to elucidate the mechan-isms for acrylamide formation in foods It has been demonstrated that acrylamide can be formed from classical Maillard reactions as well as from reaction
of the fatty acid oxidation product acrolein with ammonia and subsequent oxidation steps The most plausible explanation for the relatively high acrylamide levels in fried potato products derives from a mechanism involving the reaction of the amino group of the amino acid asparagine with the
Trang 4carbonyl group of a reducing sugar such as glucose
during baking and frying This mechanism is shown
in Figure 2 Potatoes are high in asparagine and in
reducing sugars, and they are commonly prepared
for consumption by frying or baking; all of these
factors help explain the relatively high levels of
acrylamide in heated potato products
Toxicological Considerations
Laboratory toxicology studies have indicated that
acrylamide is carcinogenic and also has been
associated with the development of reproductive
toxicity, genotoxicity, and neurotoxicity
Epidemio-logical and analytical studies of people exposed to
acrylamide in the workplace have indicated that
acrylamide does indeed enter the bloodstream of
workers and can be detected and quantified as
hemoglobin adducts, thus indicating both exposure
and absorption of acrylamide Such studies have not,
however, indicated increases in cancer rates among
those exposed occupationally to acrylamide To
date, the only documented toxicological effect
observed in epidemiological studies of workers
exposed to acrylamide is neurotoxicity This effect
is primarily an acute effect caused by large
expo-sures to acrylamide for relatively short periods of
time, leading to nervous system damage, weakness,
and incoordination of limbs
From a biochemical standpoint, it is likely that the
health effects caused by high levels of exposure in
humans and in laboratory animals may result from a
Michael-type nucleophilic addition reaction of
amino acids (both amino and sulfhydryl groups),
peptides, and proteins to acrylamide because of the
presence of the ,-unsaturated conjugated structure
in acrylamide This is a common toxicological
path-way for many reactive compounds It is likely that
high doses of acrylamide may overwhelm the
defen-sive mechanisms of the body such as glutathione
conjugation and may cause reaction with biologi-cally significant nucleophiles, leading to mutations and possible carcinogenicity
Although it is clear that humans have been con-suming significant amounts of acrylamide in their diets for a long time, the relatively new discovery
of acrylamide as a food contaminant has raised several questions Significant efforts are currently being made to better understand the levels of acry-lamide throughout the food chain and to estimate dietary exposure to acrylamide In addition, there is much emphasis on developing food processing approaches that can reduce acrylamide formation Regulatory limits for acrylamide in food have yet
to be established since dietary acrylamide risk assessments are still being developed In the mean-time, the FDA recommends that consumers eat a balanced diet that includes a wide variety of foods low in trans fat and saturated fat and rich in high-fiber grains, fruits, and vegetables
Perchlorate
Perchlorate exists as an anion (ClO4) with a central chlorine atom surrounded by four oxygen atoms arranged in a tetrahedron Perchlorate is manufac-tured in the United States and is used as the primary ingredient of solid rocket propellant Perchlorate wastes from the manufacture and/or improper dis-posal of perchlorate-containing chemicals are fre-quently detected in the soil and water Levels of perchlorate have been detected in 58 California pub-lic water systems and in water samples from 18 states
The widespread water contamination by perchlo-rate and its potential to cause health effects in those consuming contaminated drinking water have led four US agencies—the EPA, Department of Defense, Department of Energy, and National Aeronautics and Space Administration—to request that the
US National Academy of Sciences convene a study
on ‘‘Toxicological Assessment of Perchlorate Ingestion.’’
Occurrence in Food Although the primary concerns from perchlorate contamination result from drinking water con-sumption, recent evidence has indicated that perchlorate may contaminate food items as well
A small survey of 22 lettuce samples purchased in northern California showed perchlorate contami-nation in 4 samples A subsequent study of California lettuce showed detectable perchlorate levels in all 18 samples tested The toxicological
+
NH 2 O
acrylamide
H 2 N
OH
O NH 2
O
asparagine
OH HO
HO
O
glucose heat,
several steps
Figure 2 Proposed mechanism for acrylamide formation in
foods.
FOOD SAFETY/Other Contaminants 343
Trang 5significance of such findings has not been
estab-lished, but the studies clearly indicate that
perchlo-rate can enter lettuce, presumably from growing
conditions in which perchlorate has contaminated
water or soil
Milk has also been shown to be subject to
per-chlorate contamination A small survey of seven
milk samples purchased in Lubbock, Texas,
indi-cated that perchlorate was present in all of the
sam-ples at levels ranging from 1.12 to 6.30 mg/l To put
such findings in perspective, the State of California
has adopted an action level of 4 mg/l for perchlorate
in drinking water, whereas the EPA has yet to
estab-lish a specific drinking water limit
Toxicological Considerations
Perchlorate is thought to exert its toxic effects at
high doses by interfering with iodide uptake into
the thyroid gland This inhibition of iodide uptake
can lead to reductions in the secretion of thyroid
hormones that are responsible for the control of
growth, development, and metabolism Disruption
of the pituitary–hypothalamic–thyroid axis by
per-chlorate may lead to serious effects, such as
carci-nogenicity, neurodevelopmental and developmental
changes, reproductive toxicity, and
immunotoxi-city Specific concerns relate to the exposures of
infants, children, and pregnant women because
the thyroid plays a major role in fetal and child
development
The ability of perchlorate to interfere with iodide
uptake is due to its structural similarity with iodide
In recognition of this property, perchlorate has been
used as a drug in the treatment of hyperthyroidism
and for the diagnosis of thyroid or iodine
metabo-lism disorders
Ammonium perchlorate was found to be
nonge-notoxic in a number of tests, which is consistent
with the fact that perchlorate is relatively inert
under physiological conditions and is not
metabo-lized to active metabolites in humans or in test
animals
Workers exposed to airborne levels of perchlorate
absorbed between 0.004 and 167 mg perchlorate per
day These workers showed no evidence of thyroid
abnormality, and a No Observed Adverse Effect
Level was established at 34 mg absorbed
perchlo-rate/day Perchlorate does not accumulate in the
human body, and 85–90% of perchlorate given to
humans is excreted in the urine within 24 h
See also: Cancer: Epidemiology and Associations
Between Diet and Cancer Fish Food Intolerance
Food Safety: Mycotoxins; Pesticides; Bacterial
Contamination; Heavy Metals
Further Reading Becher G (1998) Dietary exposure and human body burden of dioxins and dioxin-like PCBs in Norway Organohalogen Compounds 38: 79–82.
Buckland SJ (1998) Concentrations of PCDDs, PCDFs and PCBs
in New Zealand retain foods and assessment of dietary expo-sure Organohalogen Compounds 38: 71–74.
Environmental Protection Agency (2001) Dioxin: Scientific Highlights from Draft Reassessment Washington, DC: US Environmental Protection Agency, Office of Research and Development.
Food and Drug Administration (2002) Exploratory Data on Acry-lamide in Foods Washington, DC: US Food and Drug Admin-istration, Center for Food Safety and Applied Nutrition Friedman M (2003) Chemistry, biochemistry, and safety of acry-lamide A review Journal of Agricultural and Food Chemistry 51: 4504–4526.
Jimenez B (1996) Estimated intake of PCDDs, PCDFs and co-planar PCBs in individuals from Madrid (Spain) eating an average diet Chemosphere 33: 1465–1474.
Kirk AB, Smith EE, Tian K, Anderson TA, and Dasgupta PK (2003) Perchlorate in milk Environmental Science and Tech-nology 37: 4979–4981.
Sharp R and Walker B (2003) Rocket Science: Perchlorate and the Toxic Legacy of the Cold War Washington, DC: Environmen-tal Working Group.
Tareke E, Rydberg P, Karlsson P, Eriksson S, and Tornqvist M (2002) Analysis of acrylamide, a carcinogen formed in heated foodstuffs Journal of Agricultural and Food Chemistry 50: 4998–5006.
Urbansky ET (2002) Perchlorate as an environmental contaminant Environmental Science and Pollution Research 9: 187–192 Zanotto E (1999) PCDD/Fs in Venetian foods and a quantitative assessment of dietary intake Organohalogen Compounds 44: 13–17.
Heavy Metals
G L Klein, University of Texas Medical Branch at Galveston, Galveston TX, USA
ª 2005 Elsevier Ltd All rights reserved.
Food that we are culturally habituated to consume is usually thought to be safe However, some foods are naturally contaminated with substances, the effects
of which are unknown Crops are sprayed with pesticides while they are being cultivated; some ani-mals are injected with hormones while being raised Meanwhile, other foods are mechanically processed
in ways that could risk contamination This article discusses food contamination with heavy metals, the heavy metals involved, their toxicities, and their sources in the environment A brief consideration
of medical management is also included Five metals are considered in this category: lead, mercury, cad-mium, nickel, and bismuth