Exposure to dinfon by-products (DBPs) of drinking water is multiroute and occurs in households serviced by municipal water treatment facilities that disinfet the water as a necesry step to halt the spread ofwaterbome infectious dise . Biom e ofthe two most abundant groups of DBPs of chloraio n, ehaled breth levels of trihalometanes (THMs) and uri levels of two haloacetic acids, were compared to exposure estimtes calculated from in-home tap water concentrations and responses to a re Mlated to water usage. B nd THM breath concentrations were uniformly low. Strong relationships were identified between the THM breath concentraions coollected after a shower and both the THM water conetration and the THM exposure from a shower, after adjusting for the ower delay time in collg the breath sample. Uinary haloacetc acd excretion rates were not correated to water concenons.Urinarytrichloroacetic acid cetion rates were corelated with ingstion eposue and that cor-
MethodsStudy design. We recruited 49 female subjects who had previously participated in a case-control study on neural tube birth defects and had a variety of potential exposures to chlorination DBPs, based on previously measured total THM concentrations in the tap water of each household (30). The subjects included individuals throughout the state of New Jersey, thus, they had received water from different water sources. The selection of subjects provided a wide range of HAA and THM exposures within the home rather than a distribution of exposures that might exist in either a single water distribution system or within the general population. Before a home visit, a new Tedlar (DuPont, Wilmington, DE) bag and urine sample collection vessel were sent to each subject with instructions on how to collect a postshower breath sample the evening or the morning before the visit and a first morning urine sample. Each subject was telephoned the day before the home visit as a reminder. to collect the breath and urine samples. The subject recorded the collection time of the postshower breath sample, the shower duration, the shower water temperature (hot, warm, or cold), the time of urine collection, and the time of the previous urination. During the home visit, the Tedlar bag and urine samples were retrieved; a background breath sample, a time of visit urine sample, an air sample, and a cold tap water sample were collected; and a 48-hr recall questionnaire was administered. The data collection was conducted between 7 February 1995 and 6 February 1996 in New Jersey.Postshower exhaled breath samples. Postshower whole-breath samples were collected by having the subject blow into a Tedlar air sampling bag at the completion of a shower. To quantify the breath levels, 1-2 liters of the breath were transferred onto a Carboxen 569 (Supelco, Inc., Bellefonte, PA) adsorbent trap using a personal sampling pump at a flow rate of 1 1/min as soon as the bag was returned to the laboratory. Storage tests demonstrated that the THMs were stable in the sampling bag for up to 48 hr. The breath sa...
The objective of this research was to examine the time- and dose- dependent disturbances in the hypothalamic-pituitary-thyroid (HPT) axis of adult male rats administered a potent coplanar (non-ortho) PCB, 3,3',4,4',5-pentachlorobiphenyl (PCB 126). Adult male Sprague-Dawley rats were administered a single oral bolus dose of 0, 7.5, 75, or 275 microg PCB 126/kg bw dissolved in corn oil. The rats were sacrificed periodically over 22 days. The 7.5-microg/kg dose induced hepatic ethoxyresorufin-O-deethylation EROD activity, but no changes were observed in hepatic uridine diphosphate glucuronyl transferases (UDPGTs) activity or serum TSH, T4, or fT4 concentrations. The two highest doses caused a modest decline in weight gain, induced hepatic EROD and UDPGT activities, increased serum TSH concentrations, and decreased serum T4 and fT4 concentrations. The amount of thyroxine glucuronide formed daily (pM/mg protein) increased linearly with the area-under-the-concentration-curve (AUCC) for PCB 126 in liver (microg/kg/day) and then slowed at the 275-microg/kg PCB 126 dose. Perturbations in the HPT axis were nonlinear with respect to PCB 126 dosing. As expected, an inverse relationship between the AUCC for serum T4 (microg/dl/day) and the AUCC for serum TSH (ng/dl/day) was observed; however, the relationship was highly nonlinear. These data support a mode of action for PCB 126 involving induction of hepatic UDPGTs by the aryl hydrocarbon receptor AhR. However, the dose-response characteristics of the HPT axis are nonlinear and complex, requiring sophisticated tools, such as PBPK models, to characterize dose response.
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