Health Stream Literature Summary - Issue 56 - December 2009

Validation of urinary trichloroacetic acid as a biomarker of exposure to drinking water disinfection by-products.
Zhang, W., Gabos, S., Schopflocher, S., Li, X.F. and Hrudey, S.E. (2009) Journal of Water & Health, 7(3); 359-371.

The ability of epidemiological studies to investigate associations between disinfection by-products (DBPs) and adverse health effects is limited by a number of factors including the accuracy of DBP exposure assessment. Validation of a biomarker of exposure would be a means of improving exposure assessment. Trihalomethanes (THMs) and haloacetic acids (HAAs) are the two most abundant DBP classes in tap water, however THMs are not suitable for use as biomarkers because of the very short persistence of THMs in the body. Trichloroacetic acid (TCAA) is one of the most prevalent HAAs found in chlorinated drinking water and is eliminated from the body more slowly than the THMs. TCAA may be a potentially useful biomarker for measuring DBP exposure by ingestion of drinking water as it has a sufficiently long elimination half-life, and an exposure-response relationship between ingestion of TCAA-containing water and urinary TCAA excretion has been demonstrated. TCAA in blood can also be formed via exposure to chloral hydrate, another common chlorination DBP. This study was conducted to validate urinary TCAA as a potential biomarker of exposure to DBPs in drinking water in a cohort of women of reproductive age.

Volunteers were recruited by advertising the study in a newsletter of the Graduate Students Association at the University of Alberta. Telephone and face-to-face interviews were conducted to recruit 52 healthy female volunteers who were of reproductive age and not pregnant. All participants lived in the City of Edmonton during the study period (May 2003-April 2004). Information collected included: demographics, sources of drinking water, volume of water consumption per day, types of drinking water and beverages, duration of shower/bath, physical activities and use of medications. Volunteers also answered questions about their detailed volumes and patterns of fluid intake and their physical activities. Volunteers received a diary booklet to complete each day and instructions for water delivery, water consumption and urine/blood collection.

The participants were randomly stratified into five sub-groups with each group receiving drinking water with a different TCAA concentration. This water was prepared by mixing tap water from City A in varying proportions (0% - Group 1 control group, 12.5% Group 2, 25% Group 3, 50% Group 4 and 100% Group 5) with TCAA-free bottled water. City A has high TCAA concentrations (mean 80 micro g/L) in contrast to Edmonton which has low TCAA concentrations in tap water (mean 6.7 micro g/L). Participants were asked to use the supplied water (3L supplied per person per day) for drinking and to store it in their refrigerator. Participants were asked to commence the study at the first Wednesday after completion of their menstrual cycle to preclude pregnancy during the experiment. Each participant ingested cold supplied tap water every day for 15 days. Daily water consumption was assessed by recording the volume of water remaining from each daily batch. Participants recorded in their diaries each day volumes of tap water and beverage consumption, and physical activities. Tap water samples from bottles were sent to a laboratory for TCAA analysis twice per week. Urine samples were collected on the 1st day before supplied tap water consumption (Exposure Day 0) and at the 2nd, 8th, 13th, 14th, 15th and 16th day after supply with tap water. The first morning urine (FMU) sample was collected and picked up within 2h and delivered to the laboratory. The volume of urine was recorded and TCAA analysed. Creatinine-adjusted (Cr-a) TCAA concentrations in urine were calculated based on urinary creatinine levels measured. Provision of blood samples was optional. Blood samples were collected at Exposure Day 0, 7, 13 and 14. Blood samples were collected within 24 hours and analysed for TCAA.

Background exposure to Edmonton tap water TCAA concentrations in urine and blood in participants was low. The geometric means were 1.4 micro g/L for urinary TCAA concentration and 9.6 micro g/L for blood TCAA concentration. The mean TCAA concentrations for 15 day tap water consumption in the four exposure groups ranged from 9.5 to 80 micro g/L and the mean amount of TCAA ingested ranged from 25 to 174 micro g/day. The urinary TCAA levels were statistically significantly higher after Exposure Day 7 compared with Exposure Day 0 and Exposure Day 1 (p less than 0.001). There were no statistically significant differences among the TCAA levels at Exposure Day 7, 12, 13, 14 and 15 (p greater than 0.05). The observed patterns of increase in Exposure Groups 3-5 were consistent with the reported TCAA elimination half-life in the literature. After the 12th day of supplied tap water consumption, TCAA levels in blood and urine samples increased significantly with increased exposure levels (p less than 0.05) in 96% of participants from Groups 2-5 as compared to the control group.

TCAA concentration in supplied tap water and urinary TCAA concentration in a single-day exposure were positively correlated with a correlation coefficient (r) value of 0.66 (p less than 0.001). A positive correlation was also observed between the amount of TCAA ingested and the amount of TCAA excreted in a single-day exposure (r value of 0.66, p less than 0.001). The correlation was stronger when urinary measures over 2 to 4 days were combined rather than using single days. Correlations between urinary TCAA concentrations, Cr-a TCAA concentrations and the amount of TCAA excreted suggested that all three measurements could be considered similar for measuring urinary TCAA excretion. There was a high correlation between blood TCAA concentration and TCAA concentration in tap water (r = 0.80, p less than 0.001). There was a modest correlation between blood TCAA concentration and urinary TCAA excretion (r=0.64, p less than 0.001).

The study showed that urinary TCAA, measured as concentration, creatinine-adjusted concentration or amount, is a valid biomarker of exposure to TCAA in drinking water. The concentration of TCAA in the blood was an even better biomarker of exposure, however urine sampling is less invasive and thus may be a more practical biomarker for field use.

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