OXIDIZED HEATED OILS'
MARTIN GROOTVELD*, CHRISTOPHER J.L. SILWOOD*, PAUL ADDIS3
Diabetes and Metabolic Medicine
and the Royal
Medicine and Dentistry
Food Science and Nutrition
St. Paul, Minnesota
BARTOLOME BONET SERRA
Facultad de Ciencias Experimentales
Universidad de San Pablo Ceu
Publication August 22, 2001
this report is to alert the foodsenice industry. particularly
the fast-food industry, of an emerging health issue. Considerable evidence has
accumulated over the past
decades that heated cooking oils, especially
pose several types
foods and even people working near deep fathers. Heat degrades polyunsatu-
rated fatty acids
toxic compounds; saturated and monounsaturated fatty acids
heat-induced degradation. Several types
humans to food-
air-borne breakdown products
heated oils including atherosclerosis, the forerunner to cardiovascular disease;
injlammatory joint disease, including rheumatoid arthritis; pathogenic conditions
of the digestive tract; mutagenicity and genotoxicity, properties that open signal
carcinogenesis; and teratogenicity, the property of chemicals that leads to the
development of birth defects. Factors that can contribute to improved oil
therefore fewer health concerns, are
literature reviewed raises serious questions concerning the willfisl addition of
large amounts of polyunsaturated fatty acids into the human diet without
ensure the protection
these fatty acids against
been supported in part
the Minnesota Agricultural Experiment Station
whom all correspondence should be addressed. TEL: 612-624-7704; FAX: 612425-
5272; E-mail: paddisQumn.edu
Nutrition Press, Inc., Trumbull. Connecticut.
heat- and oxidative-degradation.
is hoped that this review will stimulate
the foodservice industry
this important area
also foster the research and development activities necessary to
reduce the exposure of humans to lipid oxidation products.
The thermally-induced oxidation of glycerol-bound polyunsaturated fatty
acids (PUFAs) in foods and culinary oils during standard frying or cooking
episodes is a process that involves the prior generation of isomeric conjugated
hydroperoxydiene (CHPD) species. These CHPDs fragment to form alkoxyl
radicals that, in turn, undergo 8-scission to generate a wide range of aldehydic
view of the extremely toxic nature of the aldehydic end-products
generated, the employment of PUFA-containing culinary oils for domestic or
commercial fryinghoking episodes poses health hazards that have recently
attracted much public and clinical interest.
Indeed, these cytotoxic agents have been implicated in the development and
progression of atherosclerosis (Steinberg and Wit-
and its associated
pathological sequelae such
ischemic heart disease and peripheral vascular
disease, and have also been shown to exert gastropathic (Jayaraj
and genotoxicological (Esterbauer
properties. These phenomena are undoubtedly attributable to the extremely
high reactivity of aldehydes with critical biomolecules (e.g., thiols such
glutathione; DNA, forming covalently-modified base adducts; and the apolipo-
protein B component of low-density lipoprotein, altering its biological
Two of the contributors of this paper,
recently reported the detection and quantification of PUFA-derived oxidation
products (notably aldehydes and their CHPD precursors)
culinary oils by high
resolution proton ('H) nuclear magnetic resonance
virtually noninvasive multicomponent analytical technique (Claxson
The influence of episodes of thermal stressing (i.e., those
that simulate their domestic or commercial usage) on the generation, nature and
concentrations of such products was also evaluated in these studies. We have
also employed this technique to probe the
absorption, metabolism and
urinary excretion of typical aldehydic lipid oxidation products in experimental
and found that such agents are indeed absorbed from the gut into the
systemic circulation, metabolized (primarily via the addition of glutathione
across their electrophilic carbon-carbon double bonds), and excreted in the urine
C-3 mercapturate conjugates (Grootveld
The foregoing findings are especially relevant in view of the trend toward
the use of vegetable oils,
a replacement for
fats, for the purpose of
frying/cooking practices. Vegetable oils, even those which have been subjected
to hydrogenation, are more labile than animal-derived lard and tallow. However,
neither a return to animal-derived cooking fats nor hydrogenated vegetable oils
is likely to provide an acceptable alternative
both are problematic with regard
to health effects (Addis
1995). The issue of
fatty acids is currently
under intense investigation and a number of potential adverse health effects have
been reported (Addis and Warner 1991; Addis
cholesterol oxidation in the frying process, it has been demonstrated that toxic
cholesterol oxidation products (COPs) readily form in heated tallow (Park and
Addis 1986a,b). Furthermore, levels of COPs in heated tallow were predictable
by the conductivity
the frying medium (Zhang and Addis 1991). Moreover,
samples of French-fries obtained daily from a fast-food restaurant over a one-
month time period displayed significant though variable levels of COPs,
including the highly atherogenic
60-cholestane trio1 (Zhang and Addis
1991). COPs have been shown to occur
the plasma lipoproteins of fasted
1989) and in chylomicrons of human subjects fed a meal
rich in fat and COPs postprandially (Emanuel
1991). A review of the
literature of the biological and health effects of COPs and other components of
thermally-stressed oils would be enormous and will not
Several reviews of this area have been published and are recommended to the
reader (Addis 1986; Addis
1993, 1995; Guardiola
response to these foregoing issues, a tallow-based frying and baking fat has been
developed by removing cholesterol and blending the cholesterol-free tallow with
corn oil, achieving
oil that tends to raise serum HDL while also lowering
serum LDL (Hayes 1996). Because
fatty acids would appear not to be a problem. The
significance of this development stems from the fact that
acids interfere with the beneficial effects of both saturated and polyunsaturated
namely, raising HDL and lowering LDL, respectively (Sundram
1997; Hayes 1996). The removal of cholesterol is
terms of reducing serum cholesterol
subjects consuming the tallowhrn oil
blend (Hayes 1996).
In the following sections of this communication we review the toxicological
hazards afforded by the ingestion of aldehydes present in thermally-stressed
and/or repeatedly-utilized PUFA-rich culinary oils, and address potential
methods to limit the production of these deleterious agents during routine frying
Peroxidation of PUFA components of low-density lipoprotein (LDL)
stimulates the subsequent production of foam cells from macrophages, a crucial
stage in the pathogenesis of atherosclerosis (Addis and Warner 1991; Van
Hinsbergh 1984), and this oxidative modification occurs from the following
sequential steps: (1) generation of aldehydes from the decomposition of pre-
formed, PUFA-derived CHPDs; and (2) alteration of the apolipoprotein
moiety’s structure via Maillard reactions involving the above carbonyl
(1989) demonstrated that
(HNE), an a,P-unsaturated aldehyde arising from the autoxidation of PUFAs,
reacted with selected
acids of apo
rendering it susceptible to uptake by
the macrophage scavenger receptor. Apo
lysine residues are readily
derivatized by aldehydic CHPD fragmentation products (Jurgens
Therefore, subsequent to their
absorption, aldehydes present in
thermally/ oxidatively-stressed frying
ingested in the diet will have the
ability to directly effect structural modification of the apo
component of LDL,
a process that induces the generation of foam cells from macrophages
hallmark of atherosclerosis.
Interestingly, Smith and Kummerow (1987) have demonstrated that the
dietary consumption of peroxidized culinary oils escalated the accumulation of
macrophages and monocytes, and previous animal feeding
studies have shown that diets containing thermally-stressed, PUFA-rich oils are
more atherogenic than those containing corresponding unheated oils. More
(1996) conducted investigations
at evaluating the
ability of oxidized dietary lipids to accelerate the development of atherosclerosis
in New Zealand White rabbits and found that such a diet increased levels of fatty
streak lesions, a “fingerprint” of atherosclerosis, by 100% compared to unheated
oils. These findings clearly indicate that the consumption of PUFA-derived
oxidation products in the diet represents a hazard to human health. Furthermore,
Kritchevsky and Tepper (1967) provided evidence for the atherogenicity of
thermally-stressed PUFA-rich oils
1967. These researchers found that
heating corn oil [PUFA-content
(w/w)] at 215C for a period of 20
substantially increased its atherogenicity, whereas the heating of olive oil [PUFA
9% (w/w)] in the same manner had no effect on its atherogenic
Figure 1 shows expanded regions of high resolution ‘H NMR spectra of a
corn (maize) oil sample acquired prior to and subsequent to heating at a
temperature of 180C for a period of
The results in Fig. 1 clearly reveal
the generation of CHPDs and their aldehydic fragmentation products during the
subjection of a commonly-utilized PUFA-laden culinary oil to episodes of
thermal stressing according to standard frying practices. Therefore, it is likely
that consumption of foods subjected to standard frying procedures is a health
concern to the consumer, especially regarding cardiovascular disease.
PROTON ('H) NMR ANALYSIS OF LIPID OXIDATION PRODUCTS IN
standard frying practices
typical spectrum is shown. Abbreviations:
lipid oxidation products correspond
labeled protons in the accompanying molecular stlllctllres
peroxydiene; trans,transconjugated hydroxyperoxydiene;
THERMALLY-STRESSED CULINARY OILS
The oxygen radical-mediated peroxidation
polyunsaturates in the knee-
joint of patients with inflammatory joint diseases (e.g., rheumatoid arthritis)
have been investigated in some detail, and elevated levels
products have been measured in inflammatory knee-joint synovial fluid,
apparent consequence of a cascade
radical reactions induced by localized
episodes of ‘oxidative stress’ in vivo. In view of their aggressive reactivity
toward many essential biomolecules, aldehydic lipid oxidation products exert
powerful pro-inflammatory actions, and Benedetti
(1980) found that
injection of a mixture of peroxidized PUFA-derived carbonyl compounds
at a concentration of only 0.15
induced a significant inflammatory response (i.e. edema) in the hind paw of rats.
(1992) used gas chromatography coupled with
spectrometric detection to determine levels of
in blood plasma of patients with rheumatoid and osteoarthritis, and found that
although concentrations of this terminal peroxidation product in the osteoarthrit-
ics’ biofluids were similar to those of healthy vqlunteers (ca. 0.10
of rheumatoid patients’ plasma were significantly greater. Although at least some
of this cytotoxic agent could arise from the oxidative degradation of PUFAs in
vivo, there may be an association between these levels and the frequency of
thermally-stressed PUFA consumption in the diet.
Several of the authors have recently investigated the pro-inflammatory
properties of control and thermally-stressed culinary oils using an appropriate
animal model system (foot pad edema in the hind paw of male Wistar albino
rats), and Fig. 2 demonstrates that preheating corn and olive oils at a tempera-
ture of 250C for a period of 60 min gives rise to a marked elevation in the pro-
inflammatory properties of these materials. The increase in edema size with time
observed for the heated
oil samples is significantly greater than that arising
from heated olive oil samples, a phenomenon explicable by the much higher
content of PUFAs in the former which, of course, give rise to the generation
aldehydic peroxidation products.
Oral administration of the a$-unsaturated aldehyde 4-hydroxy-rrans-2-
nonenal to rats at a dose level of only 0.26
a concentration similar to that
of healthy human blood plasma,
been found to induce peptic ulcers in the
1986). Therefore, dietary consumption of such agents,
present at extremely high levels in thermally-stressed PUFA-rich culinary oils,
may account for a high fraction of such gastopathic conditions in humans.
In contrast to the acute toxicity observed shortly after the systemic
administration of CHPDs (experimental animals dying from severe lung damage
within 24 h), oral administration of these primary lipid oxidation products were
found to be nonlethal, a phenomenon indicating that they fail to be effectively
absorbed across the gastric or intestinal epithelium. However, it is important to
note that isomeric CHPDs could also give rise to gastropathic conditions in
humans consuming culinary oils subjected to domestic or commercial frying
Further toxicological investigations regarding thermally-stressed culinary
oils and fats have focussed on their mutagenic properties. Indeed, recent studies
(1999) and Zhong
(1999) have shown that volatile emissions
from heated culinary oils utilized for the purpose of Chinese-style cooking
mutagenic and exposure to such indoor air pollution may render humans to
increased risk of contracting lung cancer. Indeed, in view of the temperatures
employed in standard frying practices
180C), such fumes are rich in
CHPD-derived volatile aldehydic fragments, including acrolein, one of the most
highly toxic crJ3-unsaturated aldehydes generated from the thermally-induced
oxidation of PUFAs.
(1995) found that volatile emissions from
unrefined Chinese rapeseed, refined U.S. rapeseed (Canola), Chinese soybean
and Chinese peanut oils contained the mutagens acrolein and formaldehyde in
addition to 1,3-butadiene and benzene, which represent important risk factors in
the etiology of lung cancer. As expected, lowering of the cooking temperature,
or pre-addition of lipid-soluble antioxidants such
(BHA) decreased the levels of these mutagenic volatile components, and,
interestingly, the mutagenicity of individual volatile emission condensates
correlated strongly with the linolenate content of the oils investigated.
Hence, the inhalation of vaporized aldehydes by subjects conducting
commercial or domestic frying practices involving PUFA-rich culinary oils
affords a potential hazard to human health.
The mutagenic properties of repeatedly-used deep-frying fats have been
previously evaluated using the Ames test (Hageman
1988). In this study,
fat samples were fractionated into polar and nonpolar fractions by column
chromatography and the former increased the number of revertants without S-9
mix in various strains, strain TA97 being the most sensitive. The mutagenic
activity of these polar fractions was positively correlated with the level of
thiobarbituric acid-reactive substances (TBARS), an observation strongly
suggesting the involvement of lipid oxidation products in mutagenicity.
The possibility that heated culinary oils might stimulate the development of
birth defects has been studied only recently.
of the contributors of this
paper, B. Serra and
Viana, have obtained evidence indicating that both
oxygen-derived free radical species can lead
to embryo malformations (Bonet
1996). These findings
are consistent with reports from other laboratories on the embryonic malforma-
tions due to oxygen-derived free radicals induced by diabetes (Eriksson and Borg
1996) and the ameliorating effects
and Eriksson 1997).
UNHEATED olive oil
HEATED olive oil
FIG. 2. PRO-INFLAMMATORY PROPERTIES
Rat (male Wistar) foot pad edema induced by application of
volumes of (A) control
(unheated) and preheated corn oil and
control and preheated olive oil
were subjected to a
min thermal saessing episode at 250C and then cooled
ambient temperature prior
Paw circumferences were measured with a cotton loop
at the hindmost spur on the
subplatar surface. Data
are the mean values of groups of
experimental animals, and the
error bars represent associated
not significantly significant;
statistically significant at the
The mechanisms of these teratogenic effects are the subject of much
speculation. Among the cell components, PUFAs are readily oxidized by free
radicals, leading to the generation of cytotoxic aldehydic fragments (Gutteridge
These compounds can cause chromosomal
process occurs in the
could lead to malformations.
study whether culinary oils oxidized
by heat, materials rich in CHPDs and aldehydes, are teratogenic in rats, we
developed the following experiment (Bonet
Pregnant rats were fed
by gavage with
of either thermally-stressed (with a content of TBARS
mmol) or nonheated sunflower
oils from day
of pregnancy until
the end of the rat gestational period.
control group was investigated.
The animals were sacrificed and the embryos examined.
the rate of
neural tube malformations, reabsorptions, crown-rump length and the number
of somites (parameters related with the embryo size and development) in the
three experimental groups are shown. Clearly, the administration of preheated
(oxidized) oil increased the mean rate of malformations from the
controls animals to a value of
The administration of nonheated oil did not
give rise to any changes in the rate of fetal malformations (the administration of
either preheated or nonheated culinary oil did not lead to any modifications
reabsorptions, crown-rump length, or the somite number). These
results demonstrate that the administration of aldehyde-containing thermally-
stressed culinary oil is highly teratogenic in the rat, and an attractive hypothesis
is that the intake of such oxidized oils during pregnancy may be partially
responsible for the neural tube defects found in humans. Differences in the type
of heated oil used in standard frying or cooking processes may also be
responsible for the differing rates of neural tube defects found among different
populations. Further investigations are required in this research area.
AND SOMITE NUMBER IN THE DIFFERENT EXPERIMENTAL GROUPS
RATE OF EMBRYO MALFORMATIONS, REABSORPTIONS, CROWN-RUMP LENGTH
Control Heated oxidized oil
132 50 105
Neural tubes malformed,
4.6 6.0 26.0
9.5 10.0 7.5
29.5ko.i 2a.6ko.2 2a.5+0.3
4.1+0.03 3.9k0.05 3.9+0.05
Several areas of research could potentially be fruitful with regard to
building upon what is currently known about the chemical breakdown and
toxicity of heated polyunsaturated oils and other frying fats. These include
surveys of foods provided in fast food restaurants, studies of improved
maintenance of oils during restaurant usage by, for example, improved use of
antioxidants, improved filtration efficiency, determining the optimum
(fat) to use in a frying operation, and in some cases development of alternative
cooking procedures i.e. those which create food with fried characteristics but in
fact do not employ oils in the cooking process. In addition, although not
specifically reviewed in this article, precooked (uncured) meats and irradiated
meats are two types of food that may well contain lipid oxidation products
similar to those in heated polyunsaturated oils and therefore parallel studies
should be conducted.
Surveys of foods are needed to ascertain the actual consumption of lipid
oxidation products by the public. Given the complexities involved, i.e. the many
different types of fats, oils and shortenings; the many types of maintenance
schedules and equipment; the numerous foods, extremely variable in composition
and properties, that are fried, such a survey would be a major undertaking but
it must be conducted. It would also be valuable to compare restaurants that are
subjected to governmental regulation regarding oil quality, specifically regulating
maximum polar materials allowable, and those that are not. Methodology used
to monitor oil quality is also an important issue. One way to insure minimum
acceptable oil quality would be to incorporate the oil quality requirements and
maintenance schedule into the restaurant's HACCP (hazard analysis critical
control point) program. The implementation of a HACCP program for frying
oils would require the development of effective quality control (rapid, simple)
tests for oil quality.
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