The Contribution of cocoa additive to cigarette smoking addiction

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Page 144 of 207 RIVM report 650270002 Phenylethylamine CONSENSUS REPORTS No data available. STANDARDS AND RECOMMENDATIONS ADI: A threshold value of 30 mg/kg for phenylethylamine has been reported (9). TWANL = MAC: No data available. TWAD =MAK: No data available. TWAUSA: No data available. STELNL: No data available. STELUSA: No data available. LTEL: No data available. TLV-C: No data available. TLV-CARCINOGENICITY: No data available. MAK-REPRODUCTION: No data available. Others: Reference value: The mean plasma phenylethylamine level in healthy volunteers was 1129.8 ± 268.1 pg/ml (n=40, age 39.3±10.3 year (mean ± standard deviation)) (10). CLASS EG Carc. Cat.: No data available. IARC-category: No data available. CEC: No data available. Critical assessment Comparison of smoking potential related daily intake of phenylethylamine with daily intake from other sources: SMOKING PHENYLETHYLAMINE INTAKE BY EATING 25 cigarettes 3 chocolate Dutch cheese sausage /day bars of 60 g (50g) (50 g) phenylethylamine (mg) 12.1 (6)* 4.0 (8) 0.45 (9) 0.9 (9) * = assuming the dry tobacco leaves weight 10 % of fresh leaves and there is no loss on phenylethylamine during processing and combustion Nothing is known about the profile of the pyrolysis/combustion products of phenylethylamine. Conclusion The estimated natural phenylethylamine amount from tobacco plant in cigarette is at least 2200 times higher than phenylethylamine from added cocoa. Therefore, it is debatable whether phenylethylamine should be considered as an additive to tobacco. The daily potential intake of phenylethylamine from cigarettes (from tobacco plant and from added cocoa) is higher than phenylethylamine intake from other sources such as chocolate, sausage or cheese. Assuming similar bioavailability and no loss by combustion, the plasma concentration reached after ingestion of phenylethylamine from chocolate sources or other food sources is expected to be lower than after
RIVM report 650270002 Page 145 of 207 Phenylethylamine exposure from cigarettes. Also, the different route of application via smoking as compared with other sources should be taken into account. Therefore, the systemic and the local effect of smoking related exposure to phenylethylamine might be a point of concern. Since nothing is known about the pyrolysis/combustion products of phenylethylamine, this may also be a point of concern. PHARMACODYNAMICS Mechanism of action Phenylethylamine is classified as a neuromodulator of dopaminergic and possibly serotonergic and noradrenergic synapses. At the molecular physiological level, phenylethylamine potentiates transmission by postsynaptic and possibly presynaptic action. As yet, no conclusive evidence for phenylethylamine receptor has been shown (11). However, there is growing body of evidence for the existence that trace amines (TA) such as phenylethylamine, tyramine and tryptamine, function independently of the classical amine transmitters and mediate some of their effects via specific receptors. A study with 3 H-phenylethylamine in rat brain suggested the possibility of a specific binding site for phenylethylamine. Recently, a family of related mammalian 15 G protein-coupled receptors was identified of which two members (TA1- and TA2receptors) have been shown to specifically bind and/or be activated by trace amines, such as phenylethylamine (12). Pulmonary system breathing frequency: no data available. tidal volume: no data available. lung compliance: no data available. airway resistance: Phenylethylamine caused an initial relaxation (at 10 -7 - 10 -5 M) of the guinea-pig isolated lung parenchymal strip followed by contraction at higher concentration (10 -4 – 10 -3 M). Phenylethylamine produced a bronchoconstriction of perfused lungs, with a mean effective concentration (EC50) (n =5) of 4.53x10 -4 M. The relaxation of phenylethylamine seems to be mediated by ß-adrenoreceptors. The contraction effect of phenylethylamine does not seem to be mediated by α-adrenergic, muscarinic, histaminergic, serotonergic or dopaminergic receptor stimulation. It is not clear which receptors are involved phenylethylamine contraction effects (13). Cardiovascular system blood pressure: Phenylethylamine increased mean aortic blood pressure, total peripheral vascular resistance, left ventricular dP/dt, and (dP/dt)/P in chloraloseanesthetized dogs. Pretreatment with phentolamine reduced the increases in aortic blood pressure and total peripheral vascular resistance produced by phenylethylamine, whereas the effects of phenylethylamine on left ventricular dP/dt and (dP/dt)/P were abolished by propranolol, but increased after phentolamine pretreatment. Furthermore, both the cardiac and vascular effects of phenylethylamine were abolished by desipramine. These results indicate that phenylethylamine exerts both positive inotropic and vasoconstrictory effects, probably by releasing endogenous norepinephrine from the adrenergic nerve endings. (The phenylethylamine dose was not mentioned in the abstract of the article) (14).
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