Health Effects

5.3.1 Health Effects

Various substances in drinking water can adversely affect or cause disease in humans, animals, and plants. These effects are known as toxic effects. Below are general categories of toxicity, based on the organs or systems in the body affected (USEPA, 2003a):

r Gastrointestinal—affecting the stomach and intestines. r Hepatic—affecting the liver. r Renal—affecting the kidneys. r Cardiovascular or hematological—affecting the heart, circulatory system, or

blood.

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r Neurological—affecting the brain, spinal cord, and nervous system. In nonhu- man animals, behavior changes can result in lower reproductive success and

increased susceptibility to predation. r Respiratory—affecting the nose, trachea, and lungs or the breathing apparatus

of aquatic organisms. r Dermatological—affecting the skin and eyes.

r Reproductive or developmental—affecting the ovaries or testes, or causing lower fertility, birth defects, or miscarriages. This includes contaminants with genotoxic

effects, i.e., capable of altering deoxyribonucleic acid (DNA), which can result in mutagenic effects or changes in genetic materials.

Substances that cause cancer are known as carcinogens and are classified as such based on evidence gathered in studies. The USEPA classifies compounds as carcinogenic based on evidence of carcinogenicity, pharmacokinetics (the absorption, distribution, metabolism, and excretion of substances from the body), potency, and exposure. Based on the weight-of-evidence descriptors, USEPA has the following classification of con- taminants (2005): (1) carcinogenic to humans, (2) likely to be carcinogenic to humans, (3) suggestive evidence of carcinogenic potential, (4) inadequate information to assess carcinogenic potential, and (5) not likely to be carcinogenic to humans.

Many of the SOCs commonly found in groundwater, such as most prevalent volatile organic compounds (VOCs) and pesticides (e.g., benzene, tetrachloroethene (PCE), trichloroethene (TCE), and alachlor) are carcinogens and have very low maximum con- taminant levels (MCLs), which are drinking water standards legally enforceable by the USEPA.

The effects a contaminant has on various life forms depend not only on its potency and the exposure pathway but also on the temporal pattern of exposure. Short-term exposure (minutes to hours) is referred to as acute. For example, a person can become seriously ill after drinking only one glass of water contaminated with a pathogen (bacteria, virus, and parasite). Longer term exposure (days, weeks, months, and years) is referred to as chronic.

The constancy of exposure is also a factor in how the exposure affects an organism. For instance, the effects of 7 days of exposure may differ, depending on whether the ex- posure was on 7 consecutive days or 7 days spread over a month, a year, or several years. In addition, some organisms may be more susceptible to the effects of contaminants. If evidence shows that a specific subpopulation is more sensitive to a contaminant than the population at large, then safe exposure levels are based on that population. If no such scientific evidence exists, pollution standards are based on the group with the highest exposure level. Some commonly identified sensitive subpopulations include infants and children, the elderly, pregnant and lactating women, and immunocompromised individ- uals (USEPA, 2003a). The most common groups of groundwater contaminants that can cause serious health effects are heavy metals, SOCs, radionuclides, and microorganisms (pathogens).

At their natural concentrations, some heavy metals play an essential role in biochem- ical processes and are required in small amount by most organisms for normal, healthy growth (e.g., zinc, copper, selenium, and chromium). Other metals such as cadmium, lead, mercury, and tin, and the semimetal arsenic are not essential and do not cause de- ficiency disorders if absent (van der Perk, 2006). If ingested in excessive quantities, vir- tually all heavy metals are toxic to animals and humans. They become toxic by forming

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complexes with organic compounds (ligands) so that the modified molecules lose their ability to function properly, causing the affected cells to malfunction or die. In acute poi- soning, large excesses of metal ions can disrupt membrane and mitochondrial function and generate free radicals. In most cases, this leads to general weakness and malaise (van der Perk, 2006). Probably the most infamous metal associated with groundwater contamination is arsenic. Exposure to naturally occurring arsenic in drinking water from groundwater sources has been widely documented in various regions of the world and has had grave health consequences for affected populations, particularly in south and southeast Asia.

According to the USEPA, human exposure to arsenic can cause both short- and long-term health effects. Short or acute effects can occur within hours or days of ex- posure. Long or chronic effects occur over many years. Long-term exposure to arsenic has been linked to cancer of the bladder, lungs, skin, kidneys, nasal passages, liver, and prostate. Short-term exposure to high doses of arsenic can cause other adverse health effects, but such effects are unlikely to occur from U.S. public water supplies that are in compliance with the arsenic drinking water standard, currently set at 0.01 mg/L (http://www.epa.gov/safewater/arsenic/basicinformation.html#three).

The Agency for Toxic Substances & Disease Registry (ATSDR) of the U.S. Department of Health and Human Services has, on its Web site, a very detailed discussion regard- ing physiologic effects of arsenic toxicity including that from drinking contaminated groundwater (http://www.atsdr.cdc.gov/csem/arsenic/physiologic effects.html). For example: “Epidemiologic evidence indicates that chronic arsenic exposure is associ- ated with vasospasm and peripheral vascular insufficiency. Gangrene of the extremities, known as Blackfoot disease, has been associated with drinking arsenic-contaminated well water in Taiwan, where the prevalence of the disease increased with increasing age and well-water arsenic concentration (10 to 1820 ppb). Persons with Blackfoot disease also had a higher incidence of arsenic-induced skin cancers.”

Since the first publication of Rachel Carson’s Silent Spring in 1962 (Carson, 2002), there has been increasing awareness that anthropogenic chemicals in the environment can ex- ert profound and deleterious effects on wildlife populations and that human health is inextricably linked to the health of the environment. The last two decades, in particular, have witnessed growing scientific concern, public debate, and media attention over the possible harmful effects to humans and wildlife that may result from exposure to chemi- cals that have the potential to interfere with the endocrine system. These chemicals, called endocrine disruptors, are exogenous substances that act like hormones in the endocrine system and disrupt the physiologic function of endogenous hormones (Wikipedia, 2007).

On its dedicated web page, the USEPA states that “Evidence suggests that environ- mental exposure to some anthropogenic chemicals may result in disruption of endocrine systems in human and wildlife populations. A number of the classes of chemicals sus- pected of causing endocrine disruption fall within the purview of the U.S. Environmental Protection Agency’s mandates to protect both public health and the environment. Al- though there is a wealth of information regarding endocrine disruptors, many critical scientific uncertainties still remain” (http://www.epa.gov/endocrine/).

The list of endocrine disruptors is very long, and it is constantly growing as new research results become available. They encompass a variety of chemical classes, in- cluding natural and synthetic hormones, pesticides, and compounds used in the plas- tics industry and in consumer products. Endocrine disruptors are often pervasive and

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dispersed in the environment, including in groundwater. Here are a few from the major groups of synthetic chemicals: persistent organohalogens (1,2-dibromoethane, dioxins and furans, PBBs, PCBs, and pentachlorophenol), food antioxidants (BHA), pesticides (majority, if not all; e.g., alachlor, aldrin, atrazine, chlordane, DDT, dieldrin, heptachlor, lindane, mirex, zineb, and ziram), and phatalates. Heavy metals like arsenic, cadmium, lead, and mercury are also endocrine disruptors in addition to their toxic effects.

In general, the health effects associated with endocrine-disrupting compounds in- clude a range of reproductive problems (reduced fertility, male and female reproductive tract abnormalities, skewed male/female sex ratios, loss of fetus, and menstrual prob- lems), changes in hormone levels, early puberty, brain and behavior problems, impaired immune functions, and various cancers (Wikipedia, 2007).

A book by Colborn et al. (1997) Our Stolen Future examines mechanisms with which certain synthetic chemicals interfere with hormonal messages involved in the control of growth and development, especially in the fetus. The associated Web site discusses scientific findings of the impacts of endocrine disrupters at low doses, emphasizing that new research on endocrine-disrupting compounds is revealing that these compounds have impacts at levels dramatically lower than that thought to be relevant to traditional toxicology. The site also includes numerous recent research examples with full reference details: http://www.ourstolenfuture.org/NewScience/newscience.htm.

Some of the more recent research regarding the dual effects and risks of multiple contaminants in drinking water is of particular concern. For example, in a study by the University of Wisconsin–Madison, researchers noted that common mixtures of pesti- cides and fertilizers can have biological effects at the current concentrations measured in groundwater. Specifically, the combination of aldicarb, atrazine, and nitrate, which are the most common contaminants detected in groundwater in agricultural areas, can influ- ence the immune and endocrine systems as well as affect neurological health. Changes in the ability to learn and in patterns of aggression were observed. Effects are most no- ticeable when a single pesticide is combined with nitrate fertilizer. Research shows that children and developing fetuses are most at risk (Porter et al., 1999; from USEPA, 2000a).

On its Web site (http://www.atsdr.cdc.gov), the ATSDR has a detailed discussion on the health effects of many SOCs that have been found in groundwater supplies.

Health-Based Screening Levels Health-based screening levels (HBSLs) are benchmark concentrations of contaminants in water that, if exceeded, may be of potential concern for human health. HBSLs are nonenforceable benchmarks that were developed by the USGS in collaboration with the USEPA and others using (1) USEPA methodologies for establishing drinking water guidelines and (2) the most recent, USEPA peer-reviewed, publicly available human- health toxicity information (Toccalino et al., 2003, 2006). HBSLs are based on health effects alone and do not consider cost or technical limitations of water treatment required to remove a contaminant (i.e., to decrease its concentration in water below detectable levels). In contrast, maximum contaminant levels (MCLs) are legally enforceable USEPA drinking water standards that set the maximum permissible level of a contaminant in water that is delivered to any user of a public water system. MCLs are set as close as feasible to the maximum level of a contaminant at which no known or anticipated adverse effects on human health would occur over a lifetime, taking into account the best available technology (BAT), treatment techniques (TTs), cost considerations, expert judgment, and public comments (USEPA, 2006).

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For carcinogens, the HBSL range represents the contaminant concentration in drink- ing water that corresponds to an excess estimated lifetime cancer risk of 1 chance in − −

1 million (10 6 ) to 1 chance in 10,000 (10 4 ). For noncarcinogens, the HBSL represents the maximum contaminant concentration in drinking water that is not expected to cause any adverse effect over a lifetime of exposure. HBSL calculations adopt USEPA assumptions for establishing drinking water guidelines, specifically lifetime ingestion of 2 L of water per day by an adult weighing 70 kg. For noncarcinogens, it also typically is assumed that 20 percent of the total contaminant exposure comes from drinking water sources and that 80 percent comes from other sources such as food and air (Toccalino, 2007). The HBSL methodology includes the final USEPA cancer classifications (USEPA, 2005a).

HBSL for known carcinogens is calculated using the following equation (Toccalino, 2007):

(70 kg body weight) × (risk level) HBSL (μg/L) = (2 L water consumed/d) × (SF [mg/kg/d] − 1 ) × (mg/1000 μg)

(5.6) where risk level is 10 − 6 to 10 − 4 risk range, and SF is the oral cancer slope factor, which

has units of (mg/kg/d) − 1 . SF is defined as an upper bound, approximating a 95 percent confidence limit, on the increased cancer risk for a lifetime exposure to a contaminant.

This estimate is generally reserved for use in the low-dose region of the dose-response relationship. If the model selected for extrapolation from dose-response data is the lin- earized multistage model, the SF value is also known as the Q1 ∗ (carcinogenic potency factor) value.

For contaminants with suggestive evidence of carcinogenic potential, HBSLs are cal- culated using the following equation for calculating lifetime health advisory (lifetime HA) values:

HBSL (μg/L) = (2 L water consumed/d)

(5.7) where RfD = reference dose in milligrams of chemical per kilogram of body

÷ RMF

weight per day RSC = relative source contribution (defaults to 20 percent in the absence of

other data) RMF = risk management factor (defaults to 10 in the absence of other data)

An oral RfD is an estimate (with uncertainty spanning perhaps an order of magnitude) of a daily oral exposure to the human population (including sensitive subgroups) that is likely to be without an appreciable risk of deleterious effects during a lifetime (USEPA, 2006). Units for RfD are milligrams per kg per day (mg/kg/d).

For noncarcinogens, HBSLs are calculated using the following equation for calculat- ing lifetime HA values:

HBSL (μg/L) =

(2 L water consumed/d)

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