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Dietary nicotine: Won't mislead on passive smoking…: New insight into myocardial protection

BMJ 1994; 308 doi: https://doi.org/10.1136/bmj.308.6920.61c (Published 01 January 1994) Cite this as: BMJ 1994;308:61
  1. J L Repace
  1. Exposure Assessment Division, Office of Research and Development, US Environmental Protection Agency, Washington, DC 20460, USA.

    EDITOR, - Domino et al have argued that the plasma cotinine concentration in non-smokers, which is taken as an index of passive smoking, may be confounded by dietary nicotine intake from vegetables of the family Solanaceae.1 They report that eggplant (aubergine) had the most nicotine of any Solanaceae. If their data are taken at face value, daily consumption of a 174 g serving of baked eggplant with gourmet tomato sauce made from puree yields a maximum dietary nicotine dose of 15 μg (table), assuming (dubiously) That nicotine does not evaporate during baking. The mean daily total intake of all vegetables, however, is about 207 g for adults in the United States.2 A diet in which the daily average vegetable intake consists 84% by weight of eggplant parmigiana is unlikely for even the most fanatical gourmet, much less an average person, whose consumption of eggplant is about 0.4% of total per capita consumption of fresh, bought vegetables.3

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    The maximum intake-achievable only if the dish was consumed raw daily-would contribute only 15% of the plasma continine concentration due to passive smoking by a typical non-smoker and 1. 5% of the plasma cotinine concentration for the most exposed non-smokers (table). However, a typical non-smoker's actual average dietary nicotine intake produces only 0.7% of a typical non-smoker's cotinine dose from passive smoking. Dietary nicotine intake does not confound cotinine in body fluids as an index of passive smoking.

    The opinions in this letter are my own.

    References

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    … unless subjects eat 90 kg tomatoes a day

    1. M J Jarvis
    1. Exposure Assessment Division, Office of Research and Development, US Environmental Protection Agency, Washington, DC 20460, USA.

      EDITOR, - The notion that nicotine from dietary sources might contribute sufficiently to measured cotinine concentrations in non-smokers as to make objective assessment of exposure to environmental tobacco smoke unreliable or impossible has been suggested more than once, most recently by Domino et al.*RF 1* This report received widespread publicity in the media, including both the BMJ and the Lancet.*RF 2,3* If the claim could be substantiated there would be important implications for investigations of the health effects of passive smoking, which have increasingly used cotinine as a quantitative marker of exposure.

      Domino et al measured low concentrations of nicotine in some vegetables of the solanaceae family and estimated that the amount of nicotine (1 (mu)g) taken in by someone eating 10 g of aubergine of 244 g of tomato would be similar to that breathed in by a non-smoker who spent three hours in a room lightly polluted by smoke. What is at issue is not the reported concentrations of nicotine in vegetables but their biological significance.

      It is known that cotinine concentrations bear a linear relation to nicotine intake and that this remains true at the low levels of exposure characteristic of passive smoking.*RF 4* At a rough approximation, a salivary cotinine concentration of 10 ng/ml corresponds to a nicotine intake of 1 mg. Thus, on Domino's figures, the 1 (mu)g of nicotine derived from 244 g of tomatoes would be expected to generate a salivary cotinine concentration of some 10 pg/ml. This is below the detection limit of even the most sensitive assays.

      I and others examined the determinants of salivary cotinine in 7 year old children in Edinburgh.*RF 5* Geometric mean concentrations were 0.2 ng/ml in children from non-smoking households, 1. 70 ng/ml where one smoker was present, and 3. 71 ng/ml where there were two or more smokers. Similar findings have been reported by others. To explain this pattern of results, dietary nicotine would have to be perfectly confounded with parental smoking. Furthermore, it would be necessary to eat the equivalent of some 90 kg tomatoes a day to give rise to the cotinine concentrations seen in children where two or more family members smoked.

      We were able to identify a number of predictors of cotinine concentrations in children from non-smoking homes. These included social class, crowding in the home, and season of the year. These effects could be readily interpreted in terms of passive smoking, but not as dietary effects. For example, higher exposures were seen in children from lower socioeconomic groups (consistent with exposure due to the generally higher levels of smoking among more deprived groups in the community), whereas higher intakes of nicotine containing vegetables would be expected in children from more advantaged backgrounds.

      Thus, while dietary nicotine has curiosity value, it is essentially irrelevant for passive smoking. As a measure of passive smoking, cotinine has enabled more precise assessment of exposure and has considerably strengthened the evidence of adverse effects on health.

      References

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