Chlorophenol exposure in harbor workers exposed to river silt aerosols.

OBJECTIVES: While dredging the river Elbe in the harbor of Hamburg, workers are potentially exposed to river silt aerosols containing organic compounds. The aim of this cross-sectional study was to determine the internal load of chlorophenols in exposed workers. METHODS: Eighty-four exposed workers and eighty-four unexposed office workers were examined. Urinary samples were analyzed for dichlorophenols, trichlorophenols, tetrachlorophenols, and pentachlorophenol (PCP). RESULTS: For exposed workers, more than 2/3 of the urinary samples were above detection limit for 2,5-dichlorophenol, 2,4/3,4-dichlorophenol, 2,4,6-trichlorophenol, and PCP. Harbor workers had significantly higher median levels of 2,5-dichlorophenol (0.6 vs. 0.4 microg/g creatinine) and PCP (1.4 vs. 1.0 microg/g creatinine) as compared to unexposed subjects. These differences remained statistically significant after adjustment for age, smoking habits, and fish consumption. CONCLUSION: Harbor workers in the harbor of Hamburg have a statistically significant higher internal load of chlorophenols than the general population. However, the internal load is within the range of exposure reported from the general population. Therefore, even though chlorophenols are found in the river silt these exposures do not seem to be the major source of the internal load among workers in the harbor of Hamburg.

Cotinine excretion (tobacco smoke biomarker) of smokers and non-smokers: comparison of GC/MS and RIA results.

With a validated GC/MS method, the tobacco smoke biomarker cotinine has been estimated in urine for 148 non-smokers (male; 43 +/- 13 years; median 5.0 micrograms/g creatinine; 95th percentile 104 micrograms/g) and 96 smokers (male; 39 +/- 12 years; 1002 micrograms/g; 2993 micrograms/g). For a subgroup of 50 persons, the GC/MS results were compared with those by a commercially available radio immunoassay. Both methods identified the same persons as non-smokers and smokers, respectively, and were closely related. For smokers, the relationship was distinctly closer than for the non-smokers (r = 0.90, p < 0.001, n = 14 vs. r = 0.41, p < 0.02, n = 36). The RIA values were 2.4 times (smokers) and 2.9 times (non-smokers) higher than the GC/MS results. This was probably caused by the cross reactivity of the RIA antibodies against other urinary nicotine metabolites, e.g. trans-3'-hydroxycotinine, and has to be taken into account to correctly compare results of studies obtained with different analytical techniques and for choosing cut-off points to discriminate between active smokers and non-smokers of between non-smokers with higher or lower exposure to environmental tobacco smoke.

Arsenic species excretion after controlled seafood consumption.

Influence of controlled consumption of marine fish on the urinary excretion of arsenite, arsenate, dimethylarsinic and monomethylarsonic acid (DMA, MMA) was investigated in two experiments. Arsenic species were separated by anion-exchange chromatography and detected with hydride-technique atomic absorption spectrometry (detection limit 1, 10, 2, 2 microg/l). Firstly, 13 probands ate different types of seafood after having refrained from any seafood for 1 week. DMA levels rose from 3.4+/-1.3 microg/g creatinine (n=12; a day before seafood) to a mean peak level of 28.2+/-20.6 microg/g (n=13; 10-23 h after; P<0.001; max. 77.7 microg/g). No other species were excreted before the meal, but small amounts of arsenite (8.5% positive; max. 1.7 microg/g) and MMA (1.2%; 1.6 microg/g) within 2 days after it (n=82). Consumption of white herring caused the highest DMA levels. Secondly, eight probands ingested white herring (dose 3.5 g/kg; DMA content 32.1+/-15.3 ng/g wet weight; n=36). No arsenite, arsenate and MMA was found in the urine or in the herring tissues. The mean DMA mass excreted after the meal (65.3+/-22.0 microg/24 h) was about 6-fold higher than the sum of base DMA excretion (3.0+/-1.7 microg/24 h) and the ingested DMA mass (7.9+/-2.7 microg). This indicates that the elevated DMA excretion after herring consumption is not caused by the metabolism of inorganic arsenic but of other arsenic species present in the fish tissue, e.g. arsenobetaine or fat-soluble arsenic species.