Disinfection by-products (DBPs) are formed when disinfectants (chlorine, ozone, chlorine dioxide, or chloramines) react with naturally occurring organic matter, anthropogenic contaminants, bromide, and iodide during the production of drinking water. Here we review 30 years of research on the occurrence, genotoxicity, and carcinogenicity of 85 DBPs, 11 of which are currently regulated by the U.S., and 74 of which are considered emerging DBPs due to their moderate occurrence levels and/or toxicological properties. These 74 include halonitromethanes, iodo-acids and other unregulated halo-acids, iodo-trihalomethanes (THMs), and other unregulated halomethanes, halofuranones (MX [3-chloro-4-(dichloromethyl)-5-hydroxy-2(5H)-furanone] and brominated MX DBPs), haloamides, haloacetonitriles, tribromopyrrole, aldehydes, and N-nitrosodimethylamine (NDMA) and other nitrosamines. Alternative disinfection practices result in drinking water from which extracted organic material is less mutagenic than extracts of chlorinated water. However, the levels of many emerging DBPs are increased by alternative disinfectants (primarily ozone or chloramines) compared to chlorination, and many emerging DBPs are more genotoxic than some of the regulated DBPs. Our analysis identified three categories of DBPs of particular interest. Category 1 contains eight DBPs with some or all of the toxicologic characteristics of human carcinogens: four regulated (bromodichloromethane, dichloroacetic acid, dibromoacetic acid, and bromate) and four unregulated DBPs (formaldehyde, acetaldehyde, MX, and NDMA). Categories 2 and 3 contain 43 emerging DBPs that are present at moderate levels (sub- to low-mug/L): category 2 contains 29 of these that are genotoxic (including chloral hydrate and chloroacetaldehyde, which are also a rodent carcinogens); category 3 contains the remaining 14 for which little or no toxicological data are available. In general, the brominated DBPs are both more genotoxic and carcinogenic than are chlorinated compounds, and iodinated DBPs were the most genotoxic of all but have not been tested for carcinogenicity. There were toxicological data gaps for even some of the 11 regulated DBPs, as well as for most of the 74 emerging DBPs. A systematic assessment of DBPs for genotoxicity has been performed for approximately 60 DBPs for DNA damage in mammalian cells and 16 for mutagenicity in Salmonella. A recent epidemiologic study found that much of the risk for bladder cancer associated with drinking water was associated with three factors: THM levels, showering/bathing/swimming (i.e., dermal/inhalation exposure), and genotype (having the GSTT1-1 gene). This finding, along with mechanistic studies, highlights the emerging importance of dermal/inhalation exposure to the THMs, or possibly other DBPs, and the role of genotype for risk for drinking-water-associated bladder cancer. More than 50% of the total organic halogen (TOX) formed by chlorination and more than 50% of the assimilable organic carbon (AOC) formed by ozonation has not been identified chemically. The potential interactions among the 600 identified DBPs in the complex mixture of drinking water to which we are exposed by various routes is not reflected in any of the toxicology studies of individual DBPs. The categories of DBPs described here, the identified data gaps, and the emerging role of dermal/inhalation exposure provide guidance for drinking water and public health research.

Occurrence, genotoxicity, and carcinogenicity of regulated and emerging disinfection by-products in drinking water: a review and roadmap for research.

Prevention of congenital cardiovascular defects has been hampered by a lack of information about modifiable risk factors for abnormalities in cardiac development Over the past decade, there have been major breakthroughs in the understanding of inherited causes of congenital heart disease, including the identification of specific genetic abnormalities for some types of malformations Although relatively less information has been available on noninherited modifiable factors that may have an adverse effect on the fetal heart, there is a growing body of epidemiological literature on this topic This statement summarizes the currently available literature on potential fetal exposures that might alter risk for cardiovascular defects Information is summarized for periconceptional multivitamin or folic acid intake, which may reduce the risk of cardiac disease in the fetus, and for additional types of potential exposures that may increase the risk, including maternal illnesses, maternal therapeutic and nontherapeutic drug exposures, environmental exposures, and paternal exposures Information is highlighted regarding definitive risk factors such as maternal rubella; phenylketonuria; pregestational diabetes; exposure to thalidomide, vitamin A cogeners, or retinoids; and indomethacin tocolysis Caveats regarding interpretation of possible exposure-outcome relationships from case-control studies are given because this type of study has provided most of the available information Guidelines for prospective parents that could reduce the likelihood that their child will have a major cardiac malformation are given Issues related to pregnancy monitoring are discussed Knowledge gaps and future sources of new information on risk factors are described

https://www.umanitoba.ca/faculties/health_sciences/medicine/units/pediatrics/sections/neonatology/media/CHD_Risk_Factors.pdf

Noninherited Risk Factors and Congenital Cardiovascular Defects: Current Knowledge: A Scientific Statement From the American Heart Association Council on Cardiovascular Disease in the Young

Extraction of natural gas from shale rock in the United States (US) is one of the landmark events in the 21st century. The combination of horizontal drilling and hydraulic fracturing can extract huge quantities of natural gas from impermeable shale formations, which were previously thought to be either impossible or uneconomic to produce. This review offers a comprehensive insight into US shale gas opportunities, appraising the evolution, evidence and the challenges of shale gas production in the US. The history of US shale gas in this article is divided into three periods and based on the change of oil price (i.e., the period before the 1970s oil crisis, the period from 1970s to 2000, and the period since 2000), the US has moved from being one of the world's biggest importers of gas to being self-sufficient in less than a decade, with the shale gas production increasing 12-fold (from 2000 to 2010). The US domestic natural gas price hit a 10-year low in 2012. The US domestic natural gas price in the first half of 2012 was about $2 per million British Thermal Unit (BTU), compared with Brent crude, the world benchmark price for oil, now about $ 80–100/barrel, or $14–17 per million BTU. Partly due to an increase in gas-fired power generation in response to low gas prices, US carbon emissions from fossil-fuel combustion fell by 430 million ton CO 2 – more than any other country – between 2006 and 2011. Shale gas also stimulated economic growth, creating 600,000 new jobs in the US by 2010. However, the US shale gas revolution would be curbed, if the environmental risks posed by hydraulic fracturing are not managed effectively. The hydraulic fracturing is water intensive, and can cause pollution in the marine environment, with implications for long-term environmental sustainability in several ways. Also, large amounts of methane, a powerful greenhouse gas, can be emitted during the shale gas exploration and production. Hydraulic fracturing also may induce earthquakes. These environmental risks need to be managed by good practices which is not being applied by all the producers in all the locations. Enforcing stronger regulations are necessary to minimize risk to the environment and on human health. Robust regulatory oversight can however increase the cost of extraction, but stringent regulations can foster an historic opportunity to provide cheaper and cleaner gas to meet the consumer demand, as well as to usher in the future growth of the industry.

Natural gas from shale formation – The evolution, evidences and challenges of shale gas revolution in United States

Objectives and methods—Chlorination has been the major disinfectant process for domestic drinking water for many years. Concern about the potential health eVects of the byproducts of chlorination has prompted the investigation of the possible association between exposure to these byproducts and incidence of human cancer, and more recently, with adverse reproductive outcomes. This paper evaluates both the toxicological and epidemiological data involving chlorination disinfection byproducts (DBPs) and adverse reproductive outcomes, and makes

https://oem.bmj.com/content/oemed/57/2/73.full.pdf

Chlorination disinfection byproducts in water and their association with adverse reproductive outcomes: a review

This review summarizes the level of epidemiologic evidence for relationships between prenatal and/or early life exposure to environmental chemical contaminants and fetal, child, and adult health. Discussion focuses on fetal loss, intrauterine growth restriction, preterm birth, birth defects, respiratory and other childhood diseases, neuropsychological deficits, premature or delayed sexual maturation, and certain adult cancers linked to fetal or childhood exposures. Environmental exposures considered here include chemical toxicants in air, water, soil/house dust and foods (including human breast milk), and consumer products. Reports reviewed here included original epidemiologic studies (with at least basic descriptions of methods and results), literature reviews, expert group reports, meta-analyses, and pooled analyses. Levels of evidence for causal relationships were categorized as sufficient, limited, or inadequate according to predefined criteria. There was sufficient epidemiological evidence for causal...

Epidemiologic evidence of relationships between reproductive and child health outcomes and environmental chemical contaminants

The effects of public drinking water contamination on birth outcomes were evaluated in an area of northern New Jersey. After excluding plural births and chromosomal defects, 80,938 live births and 594 fetal deaths that occurred during the period 1985-1988 were studied. Information on birth outcome status and maternal risk factors was obtained from vital records and the New Jersey Birth Defects Registry. Monthly exposures during pregnancy were estimated for all births using tap water sample data. Odds ratios of > or = 1.50 were found for the following: total trihalomethanes with small for gestational age, central nervous system defects, oral cleft defects, and major cardiac defects; carbon tetrachloride with term low birth weight, small for gestational age, very low birth weight, total surveillance birth defects, central nervous system defects, neural tube defects, and oral cleft defects; trichloroethylene with central nervous system defects, neural tube defects, and oral cleft defects; tetrachloroethylene with oral cleft defects; total dichloroethylenes with central nervous system defects and oral cleft defects; benzene with neural tube defects and major cardiac defects; and 1,2-dichloroethane with major cardiac defects. Total trihalomethane levels > 100 ppb reduced birth weight among term births by 70.4 g. By itself, this study cannot resolve whether the drinking water contaminants caused the adverse birth outcomes; therefore, these findings should be followed up utilizing available drinking water contamination databases.

Jorge Esmart

Papers

Public Drinking Water Contamination and Birth Outcomes