Arsenic compounds were determined in 21 urine samples collected from a
male volunteer, The volunteer was exposed to arsenic through either c
onsumption of codfish or inhalation of small amounts of (CH3)(3)As pre
sent in the laboratory air, The arsenic compounds in the urine were se
parated and quantified with an HPLC-ICP-MS system equipped with a hydr
aulic high-pressure nebulizer. This method has a determination limit o
f 0.5 mu g As dm(-3) urine. To eliminate the influence of the density
of the urine, creatinine was determined and all concentrations of arse
nic compounds were expressed in mu g As g(-1) creatinine, The concentr
ations of arsenite, arsenate and methylarsonic acid in the urine were
not influenced by the consumption of seafood, Exposure to trimethylars
ine doubled the concentration of arsenate and increased the concentrat
ion of methylarsonic acid drastically (0.5 to 5 mu g As g(-1) creatini
ne), The concentration of dimethylarsinic acid was elevated after the
first consumption of fish (2.8 to 4.3 mu g As g(-1) creatinine), after
the second consumption of fish (4.9 to 26.5 mu g As g(-)1 creatinine)
and after exposure to trimethylarsine (2.9 to 9.6 mu g As g(-1) creat
inine), As expected, the concentration of arsenobetaine in the urine i
ncreased 30- to 50-fold after the first consumption of codfish, Surpri
singly, the concentration of arsenobetaine also increased after exposu
re to trimethylarsine, from a background of approximately 1 mu g As g(
-1) creatinine up to 33.1 mu g As g(-1) creatinine. Arsenobetaine was
detected in all the urine samples investigated, The arsenobetaine in t
he urine not ascribable to consumed seafood could come from food items
of terrestrial origin that-unknown to us-contain arsenobetaine. The p
ossibility that the human body is capable of metabolizing trimethylars
ine to arsenobetaine must be considered. (C) 1997 by John Wiley & Sons
, Ltd.