Aliphatic Aldehydes Produced by Heating Chinese Cooking Oils

Lin, Jung‐Hsin; Liou, Su‐Er

doi:10.1007/s0012800076

Cited by 34 publications

(14 citation statements)

References 9 publications

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“…At 300°C, the average yield of total aliphatic aldehydes is less than 0.5 mm⅐mg Ϫ1 ⅐min Ϫ1 from most types of oil (5,12). The average yield of total aldehydes from soybean and lard oil at 150°C, however, is ϳ1.5 ppm⅐mg Ϫ1 ⅐min Ϫ1 , indicating that components of lard are pyrolyzed at lower temperatures (12).…”

Section: Discussionmentioning

confidence: 99%

“…The average yield of total aldehydes from soybean and lard oil at 150°C, however, is ϳ1.5 ppm⅐mg Ϫ1 ⅐min Ϫ1 , indicating that components of lard are pyrolyzed at lower temperatures (12). Pork lard at temperatures of 350 -400°C produces the highest amount of formaldehyde (10.9 mm ⅐ mg Ϫ1 ⅐ min Ϫ1 ), acetaldehyde (1.04 ppm ⅐ mg Ϫ1 ⅐ min Ϫ1 ), and acrolein (0.66 ppm⅐mg Ϫ1 ⅐min Ϫ1 ) via thermolytic decomposition and oxygenation of saturated fatty acids (5).…”

Section: Discussionmentioning

confidence: 99%

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Substance P acts via the neurokinin receptor 1 to elicit bronchoconstriction, oxidative stress, and upregulated ICAM-1 expression after oil smoke exposure

Li¹,

Chen²,

Chang³

et al. 2008

American Journal of Physiology-Lung Cellular and Molecular Phys

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Li P-C, Chen W-C, Chang L-C, Lin S-C. Substance P acts via the neurokinin receptor 1 to elicit bronchoconstriction, oxidative stress, and upregulated ICAM-1 expression after oil smoke exposure. Am J Physiol Lung Cell Mol Physiol 294: L912-L920, 2008. First published March 7, 2008 doi:10.1152/ajplung.00443.2007.-This study aimed to 1) assess whether substance P (SP) acts via neurokinin (NK)-1 and NK-2 receptors to stimulate neurogenic inflammation (indicated by formation of ICAM-1 expression and oxidative stress) following oil smoke exposure (OSE) in rats; and 2) determine if pretreatment with antioxidants ameliorates the deleterious effects of OSE. Rats were pretreated with NK-1 receptor antagonist CP-96345, NK-2 receptor antagonist SR-48968, vitamin C, or catechins. OSE was for 30 -120 min. Rats were killed 0 -8 h later. Total lung resistance (RL), airway smooth muscle activity (ASMA), lung ICAM-1 expression, neurogenic plasma extravasation (via India ink and Evans blue dye), bronchoalveolar lavage fluid SP concentrations, and reactive oxygen species formation [via lucigenin-and luminalamplified chemiluminescence (CL)] were assessed. Lung histology was performed. SP concentrations increased significantly in nonpretreated rats following OSE in a dose-dependent manner. RL and total ASMA increased over time after OSE. Vitamin C and catechin pretreatments were associated with significantly reduced lucigenin CL 2 and 4 h after OSE. Pretreatment with catechins significantly reduced luminal CL counts 4 and 8 h after OSE. Evans blue levels were significantly reduced following 60 and 120 min of OSE in catechinand CP-96345-pretreated rats. ICAM-1 protein expression was significantly decreased in all pretreatment groups after OSE. Thickening of the alveolar capillary membrane, focal hemorrhaging, interstitial pneumonitis, and peribronchiolar inflammation were apparent in OSE lungs. These findings suggest that SP acts via the NK-1 receptor to provoke neurogenic inflammation, oxidative stress, and ICAM-1 expression after OSE in rats.reactive oxygen species; intracellular adhesion molecule-1; acute lung injury ACTIVATION OF NONMYELINATED bronchopulmonary C-fiber endings by various stimuli [including cigarette smoke (9), airway surface osmolality changes (14), and fire smoke (22)] causes the release of tachykinins and calcitonin gene-related peptide neuropeptides stored in the peripheral nerve terminals, eliciting both central nervous system (CNS) and local axon reflex responses (4). The CNS reflex consists of bronchoconstriction, expiratory apnea, rapid shallow breathing, cough, hypotension, and bradycardia, whereas the axon reflex response initiates local inflammation, increased mucous secretion, and bronchoconstriction. Substance P (SP), a tachykinin neuropeptide, induces a range of neuroimmunogenic effects on target smooth muscle or parasympathetic ganglia cells expressing neurokinin (NK)-1 or NK-2 receptors (1, 2). These effects, collectively termed neurogenic airway inflammation, comprise bronchoconstriction, microvasc...

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Substance P acts via the neurokinin receptor 1 to elicit bronchoconstriction, oxidative stress, and upregulated ICAM-1 expression after oil smoke exposure

Li¹,

Chen²,

Chang³

et al. 2008

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…A few cooking activities, such as combusting fuel and heating oil, are known to emit carbonyls. [5][6][7][8][9][10][11] Different cooking fuels ranging from natural gas, liquefied petroleum gas, and kerosene to coal invariably produce formaldehyde and acetaldehyde. 6 The heating of fats and oils in the presence of air causes partial conversion of fats and oils to volatile chain-scission products.…”

Section: Introductionmentioning

confidence: 99%

“…6 The heating of fats and oils in the presence of air causes partial conversion of fats and oils to volatile chain-scission products. [7][8][9][10][11] Carbonyls are among these volatile emission products. Formaldehyde, acetaldehyde, acrolein, and nonanal are typically the more abundant carbonyls observed during cooking operations that use oils.…”

Section: Introductionmentioning

confidence: 99%

Carbonyl Emissions from Commercial Cooking Sources in Hong Kong

Wang

Chu

et al. 2006

Journal of the Air & Waste Management Association

117

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Cooking fumes are an important carbonyl emission source, especially in a highly urbanized city, such as Hong Kong. Cooking exhaust from 15 commercial kitchens of a variety of cooking styles was sampled and analyzed for a suite of 13 carbonyl compounds. Carbonyl compositions were varied among the different cooking styles. Formaldehyde was generally the most abundant carbonyl, and its contribution to the total carbonyl amount on a molar basis ranged from 12 to 60%. Acrolein was also found to be an abundant carbonyl in the cooking exhaust. The highest contribution by acrolein to the total carbonyls was found to be 30% in the exhaust of a western-style steak restaurant. Long-chain saturated carbonyls, that is, heptanal, octanal, and nonanal, accounted for a significant fraction (Ͼ40%) of the total carbonyls in kitchens that always used heated cooking oils. Two dicarbonyls, glyoxal and methylglyoxal, had a various presence in the cooking emissions, ranging from negligible to 10%. The presence of benzaldehyde and tolualdehyde was mostly negligible in the sampled kitchen exhaust. Annual emission rates of both individual carbonyls and total carbonyls were estimated for various types of commercial kitchens. Local-style fast-food shops contributed the highest total carbonyl emissions per year mainly because of the large number of this kind of restaurant in Hong Kong. The citywide annual emission rates of the three most toxic carbonyls, formaldehyde, acetaldehyde, and acrolein, were estimated assuming that the limited number of sampled restaurants were representative of the average restaurants. Such estimates of carbonyl emission rates were comparable to the estimated carbonyl emissions from vehicular sources, suggesting the importance of commercial cooking as a source for carbonyls in Hong Kong.

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“…Another possible mechanism describes that acrylic acid arises directly from the decomposition of two common amino acids, alanin and aspartic acid. Acrolein is also being formed in various concentrations in the pyrolysis of triglycerides (not via glycerol) and depending on the kind of cooking oil heated and the temperature applied to the oil [15].…”

Section: Mechanism Of the Formation Of Acrylamidementioning

confidence: 99%

Deep frying: the role of water from food being fried and acrylamide formation

Gertz

Klostermann

Kochhar

2003

OCL

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Summary :The formation of acrylamide during food frying is generally influenced by food type, thermal treatment and equipment. The acrylamide concentration is increased when frying oils containing a higher level of polar materials or silicone or larger amounts of diglycerides. This effect may be caused by moisture escaping from food that has an enhancing effect on the heat transfer. It was noticed that if the moisture in the frying operation was bound by special adsorbents, the acrylamide content could be reduced by more than 50%. The effects of several additives like citric acid on the formation of acrylamide during frying of chips were also investigated. The mechanism of acrylamide formation in fried foods is discussed to explain these findings.

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Aliphatic Aldehydes Produced by Heating Chinese Cooking Oils

Cited by 34 publications

References 9 publications

Substance P acts via the neurokinin receptor 1 to elicit bronchoconstriction, oxidative stress, and upregulated ICAM-1 expression after oil smoke exposure

Substance P acts via the neurokinin receptor 1 to elicit bronchoconstriction, oxidative stress, and upregulated ICAM-1 expression after oil smoke exposure

Carbonyl Emissions from Commercial Cooking Sources in Hong Kong

Deep frying: the role of water from food being fried and acrylamide formation

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