Arsenic and Old Laws
A Scientific and Public Health Analysis of Arsenic Occurrence in Drinking Water, Its Health Effects, and EPA's Outdated Arsenic Tap Water Standard
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AN OVERVIEW OF THE SCIENTIFIC AND HEALTH ISSUES RAISED BY ARSENIC REGULATION
WHAT ARE THE KEY SCIENCE AND HEALTH ISSUES FOR ARSENIC REGULATION IN TAP WATER?
There are several important public health issues raised by the presence of arsenic in Americaís tap water, including:
(These issues are discussed in this chapter.)
- Why should the public care about arsenic in drinking water?
- What are some of the environmental and biological characteristics of arsenic that are important to human health?
- What are the adverse health effects of the various chemical forms of arsenic found in U.S drinking water?
- Who in America is at special risk for adverse health effects from arsenic?
(These issues are discussed in the following chapter.)
- What can we conclude about the adequacy of the U.S. EPAís current drinking water standard for arsenic?
- What can we conclude about the adequacy of other regulatory guidelines or standards for arsenic, for example the EPA reference dose (RfD) for ingested arsenic?
- What can we conclude about what a health-protective level of arsenic in American drinking water supplies should be to prevent cancer and noncancer effects in American populations?
- How can we prevent arsenic from getting into drinking water, or remove it from drinking water once itís there?
ANALYSIS AND DISCUSSION
Why should the public care about arsenic in its drinking water?
Arsenic is an element of the earth's crust that has many economic and industrial uses. However, it also is highly toxic in many of its chemical forms, even at the low concentrations often found in drinking water. Arsenic itself, as the core element in various arsenic compounds, remains unaltered even though it may bind or unbind with other elements or undergo changes in valence, or charge state. This scientific reality has many implications for how the element moves through the human environment and how we can effectively regulate it.
Some drinking water arsenic comes from contamination by human activities. For example, arsenic can be released by industrial or mining waste sites, or can seep from a pesticide dump site into groundwater serving as a community water source. Other drinking water arsenic occurs naturally. Thus, water supplies from wells drilled into groundwater aquifers that can be laced with geochemical arsenic.
In fashioning remedies to the problem of arsenic contamination in drinking water, it may be important to consider the origin of the arsenic. But no matter the source of arsenic, public health concerns dictate that the problem be solved promptly. Where the arsenic contamination is from human activity, waste cleanups (such as Superfund cleanups) may solve the problem, while in other cases the only remedy available may be arsenic removal at the drinking water treatment plant. The bottom line is that as a matter of community and preventive medicine, we must seek to minimize or prevent adverse health effects and risks from arsenic in tap water.
What are some of the environmental and biological characteristics of arsenic that are important with respect to its effects on human health?
Tap water is one important way that people are exposed to arsenic, but they may also encounter arsenic in other environmental media, such as food, dust, soil, and ambient air. Toxic forms of arsenic are harmful to people no matter how they get into our bodies. Water can be the predominant source of the toxic forms of arsenic for many Americans, but in order for arsenic to be a health concern, it is not necessary that drinking water be the sole or dominant source of human arsenic intake. In other words, arsenic levels in our blood increase no matter what the source, so more arsenic in toxic forms from tap water or any other source increases our health risk.
This environmental and biological reality prevents our viewing tap water arsenic in isolation. If we chose to quantify health risks only for drinking water arsenic and did not consider suspected or known contributions from other human arsenic intake sources, we might well be underestimating overall or aggregate health risks. That is, our risk numbers would be at the low end of the likely range of risk numbers with all sources accounted for. This view, however, does not invite the industries responsible for arsenic in one medium to point the finger at other sources as deserving either sole or more regulatory control. For one thing, some media lend themselves more readily to effective control of environmental contaminants and associated human exposures than others. This multimedia, integrated risk concept is particularly critical in the case of drinking water arsenic. Tap water arsenic is more easily controlled through centralized regulation, for example, controls on community water supplies, than arsenic in various dispersed sources and pathways, such as arsenic in soils, arsenic in home remedies popular in certain cultures, contaminated garden crops, or localized air arsenic emissions from smelters. Consequently, the regulatory attention given to arsenic in water is especially critical.
One characteristic of drinking water arsenic of special concern to regulators and scientists is the elementís typical occurrence in an especially toxic form, inorganic oxyarsenic. Oxyarsenic occurs in two different charge states (or valences) of importance here: pentavalent, which has five valence electrons (essentially points at which other chemical groups can attach to it), and trivalent, which has three such valence electrons, or attachment points. These forms are associated with a variety of cancer and noncancer toxic effects in humans. A wealth of recent health and scientific data identify trivalent and pentavalent oxyarsenic as equally toxic under the typical long-term, lower-level exposures to these arsenicals sustained by human populations. Earlier, crude studies in which test animals were fed large quantities of either valency form under acute, that is, very short-term, conditions seemed to show some difference in the way the animalsí metabolisms reacted, but we now know that result mainly related to the high-dose, short-time conditions of the studies. These conditions do not apply to long-term exposures of human populations to lower, but still toxic, exposure levels.
Most Americans are adept at recognizing visible or "macro-scale" acute and chronic (continuing) hazards to their health and readily accept the usual characterizations of those hazards by experts. Examples include acute injuries from fire and various chronic diseases linked to smoking. But many people are less aware of environmental contaminants and their toxic potentials. Many toxic contaminants such as arsenic occur in the environment at extremely low concentrations, yet these levels still can be high enough to be of health concern because they can be toxic at trace (part-per-million, ppm) or ultra-trace (part-per-billion, ppb and part-per-trillion, ppt) levels. In some cases, the injuries to human health from exposure to contaminants may only be seen after persistent contact with the contaminant for years or even decades; in other cases, complex medical and laboratory tests must be done to establish their presence.
What are the adverse health effects of arsenic in those chemical forms likely to occur in Americaís drinking water?
The publicís perception of arsenic is still largely literary and forensic (stemming from such classics as the Joseph Kesselring play Arsenic and Old Lace and the film it inspired), and is most often recognized as the poison of choice for homicide, suicide, and other nefarious activities. This perception of arsenic toxicity represents only its most severe form. Such poisonings are acute, triggered by ingestion of very high amounts of inorganic arsenic (such as oxyarsenic) over a short time. When arsenic is ingested in large amounts deliberately or inadvertently, it produces a constellation of severe and often fatal injuries to the cardiovascular, gastrointestinal and nervous systems. This report examines the less-dramatic (but perhaps more important overall) dose-response and public health implications of widespread lower-level arsenic exposure of populations or their subsets.
We are concerned with arsenic exposures and toxic responses that are long term, occur at relatively much lower doses than those producing acute, fatal poisoning, and affect entire populations or population segments rather than a toxic outcome reported for a specific individual. In fact, we now know that the levels of arsenic and other elements in the environment that are toxic are so low that scientists could not previously have anticipated adverse effects without the growing scientific database of human epidemiological, experimental animal, and toxicological mechanistic studies. This large and evolving database defines significant toxic risks across a wide spectrum of doses or exposures.
The available information on the adverse health effects of arsenic in drinking water and in other media are to be found in various authoritative expert consensus documents listed in this paperís illustrative bibliography. These include documents of federal agencies such as the EPA, and independent scientific bodies such as the National Academy of Sciences (NAS). These treatises and individual critical reviews and research papers form the foundation of the analyses and conclusions presented in this paper. This analysis and its conclusions about the impact of tap water arsenic on public health are focused on adverse effects associated with the elementís toxicological character. Some experimental animal studies of arsenicís biological activity in recent years have suggested a potential role for the element as a nutrient in those animal species tested. Nutrient roles at very low intakes and toxic effects at higher intakes are not uncommon with environmental elements and do not, in any way, ease the need for control of excessive exposures. A nutrient role in humans, within the framework of the battery of widely accepted criteria to establish such roles, has not been determined for arsenic.
Indeed, the NASís recent report on arsenic in drinking water notes that "studies to date do not provide evidence that arsenic is an essential element in humans or that it is required for any essential biochemical process." (NAS, 1999, p. 259) Any nutrient role would have to be at very low levels, in common with other elements with dual bioactivity. It is highly unlikely that arsenic could ever be regulated to levels so low that any yet-to-be-established human deficiency for the element would occur. This topic was discussed in detail by the author elsewhere (Mushak, 1994).
Arsenic-Induced Skin and Internal Cancers
Long-term exposure of nonoccupational human populations to environmental arsenic is associated with skin cancer and with various internal cancers, such as bladder, kidney, liver, and lung cancer. The NASís 1999 report on arsenic in drinking water concluded that arsenic is "known" to cause skin, bladder and lung cancer, and noted that there is substantial evidence that arsenic in drinking water is associated with other cancers, including cancers of the liver and kidney.
Workers encountering airborne arsenic in the workplace are known to be at high risk for lung cancer and possibly other cancers as well. Nonworker populations who have been intensely studied for increased prevalence and incidence of skin and internal cancers, and whose cancer histories underlie the calculations of cancer risks for Americans exposed to drinking water arsenic, received their cancer-causing arsenic exposures from arsenic in drinking water. Consult the bibliography for further details. Among the key references are the 1984 EPA health assessment document for arsenic, the 1988 EPA assessment of some specific issues for arsenic and human health, the EPA 1996 document for arsenic health assessment, and the 1999 NAS detailed report on cancer and other adverse effects, Arsenic in Drinking Water.
Some of the most compelling evidence for arsenic as a carcinogenic (cancer-causing) substance is to be found in various studies of a large Taiwanese population exposed to arsenic in their drinking water. Also compelling are data showing elevated cancer rates in people who drank arsenic-contaminated water in Argentina and Chile. The Taiwanese study population was huge, numbering more than 40,000 subjects, and included a large control population with more than 7,000 individuals. Study groups of these sizes in the environmental epidemiology of toxic elements are not very common. The earliest cancers appearing in these Taiwanese and in other groups were skin cancers -- consisting of various histopathological types -- followed later in their lives by cancers of internal organs -- bladder, kidney, liver, lung. Arsenic-associated skin cancers occur in specific body areas not exposed to sunlight: the trunk, soles, and palms. Therefore, arsenic cancer lesions can be distinguished from cancers caused by sun exposure.
Additional strong evidence that arsenic in drinking water causes cancer is from Chile, where a larger population was studied than that in Taiwan, China -- more than 400,000 people. Researchers evaluating this Chilean population found marked increases in mortality for bladder and lung cancer in particular. Approximately 7 percent of all deaths over age 30 could be attributed to arsenic (Smith AH et al. 1998).
Some regulators and others have argued that the threat to life caused by arsenic-associated cancers differs between skin cancers and cancers of the bladder, kidney, liver, or lung. They argue that the latter cancers collectively offer a higher mortality risk and are therefore more life-threatening. This distinction is hardly reassuring, nor does it counsel neglect of skin cancer as a public health concern. Only some of the arsenic-associated cancers arising in skin and associated with arsenic are benign (the basal cell lesions) while the squamous cell carcinomas may metastasize to other organs. In any event, the findings of internal organ cancers in reports that are more recent than those for skin cancers have significantly reinforced public health and safety concerns associated with arsenic.
While some regulators have suggested that skin cancer should be downgraded as a health concern because it sometimes is not fatal, is inappropriate to consider only fatal cancers in assessing arsenicís risks to public health. Nonfatal cancers inflict enormous emotional and economic costs to the victims of these cancers, their families, and society as a whole.
Not surprisingly, new findings on arsenic carcinogenesis have generated a number of recent studies, such as ones looking at how representative the Taiwanese population data are for risk analyses in U.S. communities exposed to arsenic in drinking water and other environmental media. Some in industry and their representatives have challenged the Taiwanese data, despite the fact that the Taiwanese data are the most extensive to date, and that rates of cancers associated with drinking water arsenic are proportional, considering varying exposure levels, to those found in other geographically distinct areas, such as Argentina and Chile.
To date, however, no one has successfully challenged the view by U.S. regulators and the NAS that the Taiwanese and Chilean studies provide strong evidence of arsenicís carcinogenicity in humans. Several appraisals of these challenges merit comment and the author noted these in a 1995 paper (Mushak and Crocetti, 1995).
Some attacks on the Taiwanese data have argued that the nutritional status and metabolic aspects of the study population put it at greater risk for toxicity from arsenic exposures than U.S. communities. However, the results of these studies have not produced any convincing challenges to the scientific validity of the data on nutritional grounds (Mushak and Crocetti, 1995). Impaired nutrition as a factor producing increased arsenic toxicity in Taiwanese, even if it were valid, is hardly an exclusionary criterion for comparisons with Americans. The argument of differential nutrition requires that we assume Americans exposed to drinking water arsenic, unlike the Taiwanese, are all well-nourished and at lower risk for arsenic toxicity. This is simply untrue. Undernutrition is a chronic public health and societal problem in America, including for those in the high-risk arsenic groups, the elderly and young children (see below).
Industry and some others have cited additional factors to argue that one cannot compare the Taiwanese exposures to arsenic to American arsenic exposures. They have claimed that other contaminants, such as alkaloids, in the Taiwanese well water are the culprits or at least co-culprits. Again, this argument is unconvincing. For example, arsenic produces cancers and other arsenic-associated effects in a number of other exposure settings comparable to the Taiwanese situation, but where alkaloidal contaminants are absent.
Others have held that the Taiwanese have genetic determinants that alter arsenic metabolism in the body, resulting in a different likelihood of cancers, but genetic predisposition to arsenic-associated cancers also remains an open issue. Some recent studies suggest that there may be genetic polymorphism (that is, many different human genetic types) in the enzyme pathway which is thought to detoxify arsenic in our body ("detoxifying biomethylation"), but such polymorphism has yet to be linked to risk differences for various cancers. Furthermore, we do not know the range of genetic diversity in Americans with respect to these arsenic methylation enzymes. Nor do we have a good handle on the mechanisms of arsenic carcinogenesis, or the metabolic transformations of the element. Research has also suggested that increased arsenic methylation may be linked to a higher cancer risk. This author first hypothesized in 1983 that the body's metabolic diversion of methyl groups away from needed bodily processes to detoxifying arsenic could be a factor in causing arsenic toxicity (Mushak, 1983). Thus, as NAS's 1999 report concluded, there is no basis on which to rest any argument that the solid body of Taiwanese data associating arsenic in tap water with several cancers, or the confirmatory data from Argentina and Chile, should be rejected.
These studies, taken together, paint a compelling picture. They have lead the NAS and many other august bodies to conclude that arsenic in drinking water is known to cause cancer in humans.
Noncancer Adverse Effects of Arsenic
Low-level arsenic exposure has other toxic effects besides cancer. Inorganic arsenic in drinking water has been associated with toxicity to the central and peripheral nervous systems, the heart and blood vessels, and various precancerous lesions in the skin, including hyperkeratosis, a pronounced scaly skin condition, and changes in pigmentation. These skin changes are so characteristic that the medical literature notes that laypeople could easily identify workers who used arsenic as a sheep-dip pesticide, simply because of their obvious skin lesions.
Ingested inorganic arsenic produces both central and peripheral nervous system effects in exposed humans. Peripheral nervous system effects on both sensory and motor nerve function mainly harm adults, while very young children are more susceptible to central nervous system effects on the brain. The effects of arsenic exposure in children may persist over the long term, based on data described in EPAís 1984 health assessment document (EPA, 1984). Irreversible toxicity must obviously be viewed much more seriously than reversible effects. Once injury has occurred, simply reducing the exposure does not undo the harm.
Exposures to arsenic in drinking water and other media also cause toxic effects on peripheral blood vessels. In its extreme form, vessel toxicity takes the form of a dry gangrene, called Blackfoot Disease, particularly noted in the more heavily exposed Taiwanese. Lower exposures were linked to a very painful peripheral blood vessel disorder in Chilean children exposed to drinking water arsenic, resembling Raynaudís Disease. The latter arises from arterial and arteriolar spasm and contractions leading to impaired blood flow and cyanosis (inadequate oxygen reaching the tissues). Studies also have linked arsenic exposure from drinking water to higher rates of diabetes.
Data from the Taiwanese studies and from studies of other populations reveal that there is a dose-response relationship for ingested water arsenic and several non-cancer toxic effects (NAS, 1999; EPA, 1984, 1996). By dose-response relationship, we simply mean that as the arsenic intake increases, both the frequency and the severity of toxic effects increase in the exposed people. This type of dose-response relationship is one of the most important pieces of evidence that health scientists use to determine that a toxic chemical actually causes a particular toxic effect. For example, scientists have documented a dose-response relationship in human populations showing that increased exposure to arsenic in drinking water causes more frequent and more severe skin lesions and serious vascular effects.
Arsenic also has been linked to injury to the cardiovascular system, a particular concern in the United States where cardiovascular diseases already are a major public health concern. Elevated arsenic exposures should be considered a potential added risk factor in addition to other widely-recognized risk factors for cardiovascular diseases.
Who in America is at special risk for adverse health effects from environmental arsenic?
Different people respond to exposure to arsenic or other toxins in different ways. The toxic responses can vary greatly, even when people are exposed to the same amount of a contaminant such as arsenic.
There are many reasons for this variability in toxic response, arising from either intrinsic factors or extrinsic causes. Intrinsic factors are those peculiar to the individual, and over which the individual has little control, for example, gender, age, race, stage of development, or group behavioral traits. Extrinsic factors are those outside the individualís characteristics and include length of exposure to a toxic substance. A general discussion of characteristics that can heavily influence the differential toxicity of toxins to different individuals, in the context of lead, is included in the NASís 1993 report on populations sensitive to lead exposure (NAS, 1993a), of which the chief author of this report was a co-author. A second NAS report appearing in 1993 (NAS, 1993b) detailed the increased sensitivity of very young children to pesticides compared to adults. As discussed below, many of the basic principles that may lead to higher risks in children from lead or pesticides (for example, childrenís immature detoxification systems and higher exposure to drinking water per unit of body weight) apply to arsenic.
Variability in the human populationís sensitivity to environmental contaminant toxicities is now an accepted principle in scientific, regulatory, and legislative quarters. This acceptance by science is found in numerous documents and individual research papers dealing with environmental contaminants, illustrated in the cited treatises and papers. Agencies such as the EPA regulate environmental metals and other contaminants with an eye to those populations at special risk, not "average" populations. That is, population segments with particular biological sensitivities or enhanced exposures are identified in relevant rulemaking for adequate protection from exposure and associated toxic harm.
In 1996 Congress enacted the Food Quality Protection Act (FQPA), Pub. L. No. 104-170, 110 Stat. 1489 (1996), partly in response to the 1993 NAS report on children and pesticides (NAS, 1993b), Pesticides in the Diets of Infants and Children. The FQPA mandates special protection for young children from pesticides, including a general requirement that an added tenfold margin be included to ensure safety for children, unless reliable data show that such an additional safety factor is unnecessary to protect children. Similarly, Congress adopted the "Boxer Amendment" in the 1996 Safe Drinking Water Act Amendments, which requires EPA to consider children, infants, pregnant women, and other especially vulnerable subpopulations in setting drinking water standards. SDWA ßß 1412(b)(1)(C), (b)(3)(C)(5), 1457(a).
We can readily identify two segments of the U.S. population that are at risk. First, older adults who have sustained elevated arsenic exposures over the long term are at special risk. Both cancer and noncancer toxic effects can occur in these individuals as a result of their prolonged exposure.
Second, very young children can be at elevated risk. The very young, especially infants and toddlers, are more likely to come into direct contact with arsenic. For instance, they often put arsenic-contaminated items in their mouths. In addition, pound for pound they consume more arsenic and other contaminants than adults. A higher arsenic intake rate for children per unit of body weight has been shown, as seen for example in the 1999 study of Calderon et al. evaluating American subjects. Additionally, the very young, being less able to defend against toxicants than are older children or adults. In the case of arsenic, we have to take into account that the very young do not detoxify arsenic as efficiently as adults, as shown in recent studies. Data from a study by Concha (1998a) indicate the fraction of toxic inorganic arsenic found in exposed childrenís urine is about 50 percent higher than it is in adult women exposed to similar levels. These investigators found that about 50 percent of the arsenic in children's urine was in the toxic inorganic form, while the adults had just 32 percent inorganic form, suggesting that children may be less able to detoxify arsenic and therefore may be more susceptible to its toxic effects. Data from a study by Kurttio et al., (1998) indicate that this differential in biomethylation-detoxification may persist over many years. We also must consider that children are more sensitive to the central nervous system effects of arsenic than adults are, and that children who sustain central nervous system injuries from arsenic may have irreversible injury, as noted above (EPA, 1984).
A third high-risk population, not fully characterized, is fetuses, which can be exposed to arsenic by way of maternal exposure. Arsenic, like a number of other environmental contaminants, crosses the placental barrier in pregnant mammals (for example, NAS, 1999). The fetus is even more biologically sensitive than the infant and toddler. Arsenic intoxication of the conceptus (human embryo relatively shortly after conception) can potentially target both organogenesis (the generation of the developing vital organs) in the embryo stage and further development in the later, fetal stage. While no in-utero arsenic effects have been documented for human exposures, we do know that oral intake of arsenic in experimental animal studies produced birth defects, impaired fetal growth, and reduced the survival of fetal and newborn animals (see, for example, NAS 1999). Of particular concern here is the recent finding that arsenic enters the fetal circulation in pregnant women by at least the third trimester, and that the level of arsenic in umbilical cord blood approaches the maternal arsenic level (Concha et al., 1998b).
Because of variations in human sensitivity to arsenic, including indications that children may be more vulnerable to this toxin, the NAS (1999) suggested that "a wider margin of safety might be needed when conducting risk assessments of arsenic because of variations in metabolism and sensitivity among individuals or groups"(p. 5). The next chapter, dealing with conclusions about the regulatory status of drinking water arsenic in America, focuses on these risk groups.
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