Exposure to drinking water disinfection by -products ( DBPs ) , such as trihalomethanes ( THMs ) , has been associated with bladder and colorectal cancer in humans. Exposure to DBPs has typically been determined by examining historical water treatment records and reconstructing study participants' water consumption histories. However, other exposure routes, such as dermal absorption and inhalation, may be important components of an individual's total exposure to drinking water DBPs. In this study, we examined individuals' exposure to THMs through drinking, showering, or bathing in tap water. Thirty -one adult volunteers showered with tap water for 10 min ( n = 11 ) , bathed for 10 min in a bathtub filled with tap water ( n = 10 ) , or drank 1 l of tap water during a 10 -min time period ( n = 10 ) . Participants provided three 10 ml blood samples: one sample immediately before the exposure; one sample 10 min after the exposure ended; and one sample 30 min ( for shower and tub exposure ) or 1 h ( for ingestion ) after the exposure ended. A sample of the water ( from the tap, from the bath, or from the shower ) was collected for each participant. We analyzed water samples and whole blood for THMs ( bromoform, bromodichloromethane, dibromochloromethane, and chloroform ) using a purge -and -trap / gas chromatography / mass spectrometry method with detection limits in the parts -perquadrillion range. The highest levels of THMs were found in the blood samples from people who took 10 -min showers, whereas the lowest levels were found in the blood samples from people who drank 1 l of water in 10 min. The results from this study indicate that household activities such as bathing and showering are important routes for human exposure to THMs.

Exposure to certain volatile organic compounds (VOCs) commonly occurs in industrialized countries. We developed a method for measuring 32 VOCs in 10 mL of whole blood at low concentration. We used this method to determine the internal dose of these compounds in 600 or more people in the US who participated in the Third National Health and Nutrition Examination Survey. From our study results, we established a reference range for these VOCs in the general population of the US. We found detectable concentrations of 1,1,1-trichloroethane, 1,4-dichlorobenzene, 2-butanone, acetone, benzene, chloroform, ethylbenzene, m,p-xylene, styrene, tetrachloroethane, and toluene in most of the blood samples of nonoccupationally exposed persons. The accuracy of VOC evaluations depends on the ability of investigators to make sensitive and reproducible measurements of low concentrations of VOCs and to eliminate all sources of interference and contamination.

Volatile organic compounds (VOCs) are an important public health problem throughout the developed world. Many important questions remain to be addressed in assessing exposure to these compounds. Because they are ubiquitous and highly volatile, special techniques must be applied in the analytical determination of VOCs. The analytical methodology chosen to measure toxicants in biological materials must be well validated and carefully carried out; poor quality assurance can lead to invalid results that can have a direct bearing on treating exposed persons. The pharmacokinetics of VOCs show that most of the internal dose of these compounds is quickly eliminated, but there is a fraction that is only slowly removed, and these compounds may bioaccumulate. VOCs are found in the general population at the high parts-per-trillion range, but some people with much higher levels have apparently been exposed to VOC sources away from the workplace. Smoking is the most significant confounder to internal dose levels of VOCs and must be considered when evaluating suspected cases of exposure.

]In July 2004, two individuals developed blisters after the destruction of a WWl-era munition. To determine the causative agent, urine samples were collected from both the highly blistered patient (patient 1; 6.5% of total body surface area) and patient 2, who had only one small blister. Their urine was analyzed for metabolites of known vesicants including sulfur mustard (HD), Lewisite (L1), and nitrogen mustards. The urine samples only tested positive for metabolites of HD. Additional metabolites were measured to confirm the exposure of sulfur mustard agent HD, including thiodiglycol (TDG), TDG-sulfoxide, and the bismercapturate of mustard sulfone. On day 2 after the exposure, patient I had a lS-lyase metabolite level of 41 ng/mL, and patient 2 had a level of 2.6 ng/mt. Detectable levels of the ~-Iyase metabolite were observed in patient 1 for 11 days and in patient 2 for 7 days. Levels of TDG and both TDG and its sulfoxide measured together in the urine of patient 1 were found to be 24 ng/mL and 50 ng/mL, respectively, on day 2. The bis-mercapturate of mustard sulfone was detected in patient 1 (3.1 ng/mL) on day 2 but was not detected in samples taken on subsequent days.The metabolism of HD has been studied extensively in rats (3,4). Research has identified several urinary metabolites, including the free and conjugated forms of the simple hydrolysis product thiodiglycol (TDG) and TDG-sulfoxide (TDG's oxidized form), the glutathione-derived metabolite 1,1'-sul- fonylbis[2-S-(N-acetylcysteinyl)ethane], and the I~-lyase metabolites 1,1'-sulfonylbis[2-(methylsulfinyl)ethane] (SBMSE) and 1-methylsulfinyl-2-[2-(methylthio)-ethylsulfonyl]ethane (MSMTESE). Although 1,]'-sulfonylbis[2-(methylthio)ethane] (SBMTE)was not identified in rat urine, it is a likely precursor to the I~-lyase metabolites that were identified (3-8).Recently, two individuals were thought to have been exposed to HD accidentally during the destruction of a WWI-era shell (9,10). The extent of blistering between the two individuals varied. One individual (patient 1) had blisters on an estimated 6.5% of his body including his hands and forearms; the second individual (patient 2) had only one small blister (9,10). Urine samples from both individuals were analyzed to confirm that the symptoms were caused by HD exposure.