Haemoglobin adducts from aromatic amines and tobacco-specific nitrosamines in pregnant smoking and non-smoking women

In non-smokers, haemoglobin adducts from 3- and 4-aminobiphenyl have been reported to arise mainly from exposure to environmental tobacco smoke (ETS). Therefore, the impact of self-reported smoking (n = 27) and exposure of non-smokers to ETS (n = 78) on haemoglobin adducts was studied in pregnant women from Homburg, Germany. In addition to 3- and 4-aminobiphenyl, adducts from seven monocyclic aromatic amines (aniline, o-, m-, and p-toluidine, 2,4-dimethylaniline, 2-ethylaniline and o-anisidine) and the adduct from tobacco-specific nitrosamines (4-hydroxy-1-(3 -pyridyl)-1-butanone) were determined. Five of 78 self-reported non-smoking women had plasma cotinine levels and urinary cotinine/creatinine ratios indicative of active smoking. In the remaining 73 non-smokers cotinine/creatinine ratios correlated significantly with self-reported exposure to ETS. However, none of the haemoglobin adducts increased with increasing exposure to ETS or increasing cotinine/creatinine ratios. Although significantly elevated in smoking compared with non-smoking women, the mean haemoglobin adduct levels formed by tobacco-specific nitrosamines (54.7 +/- 8.9 vs 26.7 +/- 4.1 fmol g(-1), p < 0.001), 3-aminobiphenyl (3.0 +/- 0.5 vs 14 +/- 0.1 pg g(-1), p < 0.001), 4-aminobiphenyl (27.9 +/- 3.4 vs 10.2 +/- 0.7 pg g(-1), p < 0.001), o-toluidine (289 +/- 25 vs 237 +/- 65 pg g(-1), p < 0.001), p-toluidine (315 +/- 32 vs 197 +/- 13 pg g(-1); p < 0.001), 2,4-dimethylaniline (25.5 +/- 2.9 vs 18.6 +/- 1.6 pg g(-1), p < 0.05), had considerable overlappings ranges indicating lack of specificity as biomarkers to tobacco smoke exposure. Exposure to other as yet unknown environmental sources appears to be more significant than previously thought.