Comparison of Trihalomethanes in Tap Water and Blood: A Case Study in the United States

Background: Epidemiological studies have used various measures to characterize trihalomethane (THM) exposures, but the relationship of these indicators to exposure biomarkers remains unclear

Assessing exposure in epidemiologic studies to disinfection by-products in drinking water: report from an international workshop.

The inability to accurately assess exposure has been one of the major shortcomings of epidemiologic studies of disinfection by-products (DBPs) in drinking water. A number of contributing factors include a) limited information on the identity, occurrence, toxicity, and pharmacokinetics of the many DBPs that can be formed from chlorine, chloramine, ozone, and chlorine dioxide disinfection; b) the complex chemical interrelationships between DBPs and other parameters within a municipal water distribution system; and c) difficulties obtaining accurate and reliable information on personal activity and water consumption patterns. In May 2000, an international workshop was held to bring together various disciplines to develop better approaches for measuring DBP exposure for epidemiologic studies. The workshop reached consensus about the clear need to involve relevant disciplines (e.g., chemists, engineers, toxicologists, biostatisticians and epidemiologists) as partners in developing epidemiologic studies of DBPs in drinking water. The workshop concluded that greater collaboration of epidemiologists with water utilities and regulators should be encouraged in order to make regulatory monitoring data more useful for epidemiologic studies. Similarly, exposure classification categories in epidemiologic studies should be chosen to make results useful for regulatory or policy decision making

Cyanobacterial Harmful Algal Blooms: Chapter 15: Cyanotoxins Workgroup Report

The Cyanotoxins Workgroup was charged with the identification and prioritization of research needs associated with: the identification of cyanotoxins; toxicokinetics and toxicodynamics of cyanotoxins; human susceptibility to the toxins; cyanobacterial genetics/omics and factors for inclusion in predictive models of toxin production; and risk reduction from an intentional or accidental release of cyanotoxins. Papers presented for the Cyanotoxins Session of the symposium on toxin types, toxicokinetics, and toxicodyamics (See Humpage this volume), cyanobacterial genetics of toxin production (See Neilan this volume), and parameters related to human risks from cyanobacterial exposure (See Love this volume) set the stage for Cyanotoxins Workgroup discussions. A consensus was achieved regarding the need to focus on the major identified classes of cyanotoxins. The group expressed the belief that the most significant toxic components of presently occurring harmful algal blooms have been identified, and the knowledge gaps for these most prevalent toxins are great enough to warrant the attention of most of our future research. This belief does not negate the need to study mixtures of cyanotoxins and toxin precursors, especially those most likely to occur within a given bloom. Moreover, there is also a significant likelihood that novel cyanobacterial blooms and toxins will continue to emerge, and future identification of unknown bloom-forming species and their toxins will require ongoing diligence

Analysis of in vivo and in vitro DNA strand breaks from trihalomethane exposure

<p>Abstract</p> <p>Background</p> <p>Epidemiological studies have linked the consumption of chlorinated surface waters to an increased risk of two major causes of human mortality, colorectal and bladder cancer. Trihalomethanes (THMs) are by-products formed when chlorine is used to disinfect drinking water. The purpose of this study was to examine the ability of the THMs, trichloromethane (TCM), bromodichloromethane (BDCM), dibromochloromethane (DBCM), and tribromomethane (TBM), to induce DNA strand breaks (SB) in (1) CCRF-CEM human lymphoblastic leukemia cells, (2) primary rat hepatocytes (PRH) exposed in vitro, and (3) rats exposed by gavage or drinking water.</p> <p>Methods</p> <p>DNA SB were measured by the DNA alkaline unwinding assay (DAUA). CCRF-CEM cells were exposed to individual THMs for 2 hr. Half of the cells were immediately analyzed for DNA SB and half were transferred into fresh culture medium and incubated for an additional 22 hr before testing for DNA SB. PRH were exposed to individual THMs for 4 hr then assayed for DNA SB. F344/N rats were exposed to individual THMs for 4 hr, 2 weeks, and to BDCM for 5 wk then tested for DNA SB.</p> <p>Results</p> <p>CCRF-CEM cells exposed to 5- or 10-mM brominated THMs for 2 hr produced DNA SB. The order of activity was TBM>DBCM>BDCM; TCM was inactive. Following a 22-hr recovery period, all groups had fewer SB except 10-mM DBCM and 1-mM TBM. CCRF-CEM cells were found to be positive for the <it>GSTT1-1 </it>gene, however no activity was detected. No DNA SB, unassociated with cytotoxicity, were observed in PRH or F344/N rats exposed to individual THMs.</p> <p>Conclusion</p> <p>CCRF-CEM cells exposed to the brominated THMs at 5 or 10 mM for 2 hr showed a significant increase in DNA SB when compared to control cells. Additionally, CCRF-CEM cells exposed to DBCM and TBM appeared to have compromised DNA repair capacity as demonstrated by an increased amount of DNA SB at 22 hr following exposure. CCRF-CEM cells were found to be positive for the <it>GSTT1-1 </it>gene, however no activity was detected. No DNA SB were observed in PRH or F344/N rats exposed to individual THMs.</p

Estimating Potential Increased Bladder Cancer Risk Due to Increased Bromide Concentrations in Sources of Disinfected Drinking Waters

Public water systems are increasingly facing higher bromide levels in their source waters from anthropogenic contamination through coal-fired power plants, conventional oil and gas extraction, textile mills, and hydraulic fracturing. Climate change is likely to exacerbate this in coming years. We estimate bladder cancer risk from potential increased bromide levels in source waters of disinfecting public drinking water systems in the United States. Bladder cancer is the health end point used by the United States Environmental Protection Agency (EPA) in its benefits analysis for regulating disinfection byproducts in drinking water. We use estimated increases in the mass of the four regulated trihalomethanes (THM4) concentrations (due to increased bromide incorporation) as the surrogate disinfection byproduct (DBP) occurrence metric for informing potential bladder cancer risk. We estimate potential increased excess lifetime bladder cancer risk as a function of increased source water bromide levels. Results based on data from 201 drinking water treatment plants indicate that a bromide increase of 50 μg/L could result in a potential increase of between 10^–3 and 10^–4 excess lifetime bladder cancer risk in populations served by roughly 90% of these plants