Overview
Health Canada’s May 2006 Guideline Technical Document for arsenic in drinking water, prepared with the Federal-Provincial-Territorial Committee on Drinking Water of the Federal-Provincial-Territorial Committee on Health and the Environment, establishes a maximum acceptable concentration (MAC) for arsenic in drinking water of 0.010 mg/L (10 µg/L) based on municipal- and residential-scale treatment achievability. The document classifies arsenic as a Group 1 human carcinogen and notes that the MAC is higher than the concentration that would represent an “essentially negligible” lifetime cancer risk (estimated at 0.3 µg/L on the basis of internal organ cancer endpoints in the southwestern Taiwan cohort). The document is identified as a risk-management decision: every effort should be made to reduce arsenic in drinking water to as low as reasonably achievable (ALARA), and the 10 µg/L MAC reflects the practical quantitation limit (3 µg/L), the reliable measurement limit (5 µg/L), and what municipal- and residential-scale treatment can practically achieve at reasonable cost, especially for smaller public systems and private wells. Lifetime cancer risk at the MAC is estimated at 3.0 × 10⁻⁵ to 3.9 × 10⁻⁴ — above the 10⁻⁶ to 10⁻⁵ range Health Canada defines as “essentially negligible.” The document compiles Canadian provincial and territorial drinking-water arsenic occurrence data from 1976 to 2002, reviews analytical methods and municipal/residential treatment technologies, and synthesizes the human and animal toxicology underlying the carcinogenicity classification.
This is the May 2006 guideline document, which supersedes prior Health Canada guideline technical documents on arsenic in drinking water (the 1989 guideline of 25 µg/L, lowered following review of the southwestern Taiwan internal-organ cancer evidence). The 10 µg/L MAC is numerically the same as the US EPA 10 µg/L MCL (see EPA — Maximum Contaminant Level for Arsenic in Drinking Water) and the WHO 10 µg/L provisional guideline; the underlying derivations are not all identical and are described in the respective agency documents.
Key numbers
Guideline values (Sections 1.0 and 11.0):
| Parameter | Value |
|---|---|
| Maximum acceptable concentration (MAC) for total arsenic in drinking water | 0.010 mg/L (10 µg/L) |
| “Essentially negligible” risk target concentration (health-based, internal organ cancer endpoints) | 0.3 µg/L |
| Practical quantitation limit (PQL, ability of laboratories to measure within reasonable limits) | 0.003 mg/L (3 µg/L) |
| Reliable measurement limit cited as basis for MAC | 0.005 mg/L (5 µg/L) |
| IARC and Health Canada carcinogen classification | Group 1 (carcinogenic to humans) |
| Mode-of-action framework used | Linear extrapolation; data deemed not strong enough to justify non-linear model |
| ALARA principle | Applies; every effort should be made to maintain arsenic levels as low as reasonably achievable |
Unit risk and lifetime cancer risk estimates (Section 10.0, Health Canada 2005 quantitative risk assessment using Poisson-Weibull model from Morales et al. 2000 fit to southwestern Taiwan data of Chen et al. 1985 and Wu et al. 1989):
| Parameter | Value |
|---|---|
| Unit risk range, per 1 µg/L arsenic, 1% extra risk basis | 3.06 × 10⁻⁶ to 3.85 × 10⁻⁵ |
| Unit risk 95% upper-bound range | 6.49 × 10⁻⁶ to 4.64 × 10⁻⁵ |
| Lower bound of range (most sensitive endpoint) | Liver cancer (3.06 × 10⁻⁶) |
| Upper bound of range (most sensitive endpoint) | Lung cancer (3.85 × 10⁻⁵) |
| Lifetime cancer risk at MAC (10 µg/L) | 3.0 × 10⁻⁵ to 3.9 × 10⁻⁴ |
| Lifetime cancer risk at “essentially negligible” target (0.3 µg/L) | 95% UCL: 1.9 × 10⁻⁶ to 1.39 × 10⁻⁵ |
| Definition of “essentially negligible” in Health Canada drinking water context | 10⁻⁶ to 10⁻⁵ (one new cancer above background per 1,000,000 to 100,000 people over lifetime) |
Estimated lifetime range of risk of excess internal organ cancers at various drinking-water arsenic concentrations (Table 1, p. 3, 70-year lifetime, additional to background, × 10⁻⁵):
| Level of arsenic in drinking water (µg/L) | Estimated lifetime range of risk of excess internal organ cancers (× 10⁻⁵) |
|---|---|
| 0.3 (“essentially negligible”) | 0.09–1 |
| 5 | 2–20 |
| 10 (MAC) | 3–39 |
| 25 | 8–97 |
Canadian drinking-water occurrence data (Section 5.1, provincial and territorial monitoring submissions):
| Jurisdiction and water type | Period | Range (µg/L) | Average / annual mean (µg/L) | Notes |
|---|---|---|---|---|
| Prince Edward Island, groundwater | 1986–2002 | 0.1–26.0 | ~1.5 | >99% of samples <10 µg/L |
| Quebec, municipal treated surface water (523 communities) | 1990–2002 | 1.0–25.0 | 1.6 | >99% of samples <10 µg/L |
| Quebec, municipal treated groundwater (562 communities) | 1990–2002 | 1.0–60 | 2.0 | ~98% of samples <10 µg/L |
| Ontario, treated groundwater and surface water (726 communities) | 1997–2002 | 0.1–18 | ≤0.7 | >99% of samples <10 µg/L |
| Ontario, private-lab treated and raw drinking water | 1999–2002 | <2.5–68 | <2.5 | Higher values predominantly from wells |
| Saskatchewan, municipal treated water (539 communities) | 1976–2002 | 0.5–105.0 | 3.0 | 97% of samples ≤10 µg/L |
| Alberta, treated groundwater and surface water (573 communities) | 1980–2002 | 0.1–1000 | 1.8 | ~99% of samples <10 µg/L |
| Nova Scotia well water (Environmental Chemistry Laboratory) | 1991–1997 | — | — | 9% of samples >25 µg/L |
| Nova Scotia 7-community study (Méranger et al. 1984) | — | — | — | Levels exceeded 50 µg/L in 33–93% of wells per community; >500 µg/L in 10% of wells (n=94) |
| Newfoundland, public water supplies (54 wells) | 2002 | 6–288 (maximum levels) | — | — |
| Newfoundland, school well-water supplies (n=16) | 2002 | 1–368 | — | ~19% had maximum levels above 10 µg/L |
| British Columbia, Bowen Island groundwater | 1998 | — | — | Maximum 580 µg/L reported |
International occurrence context (Section 5.1):
| Region | Reported level |
|---|---|
| Western US states with volcanic rock/sulphidic mineral deposits | >3 mg/L in groundwater (ATSDR 2000) |
| Argentina, Buenos Aires Province (Médanos) | Up to 2 mg/L |
| Argentina, Córdoba (La Francia) | Up to 12 mg/L |
Estimated mean daily intake of total arsenic from food (Section 5.2):
| Population | Total arsenic intake (µg/day) | Range |
|---|---|---|
| Adults 20–65+, Canada (Dabeka 1993) | 42 | 22.5–78.7 |
| Adults 25–70+, United States (Tao and Bolger 1998) | 56 | 27.5–92.1 |
| Adults, United Kingdom (MAFF 1999) | 120 | — |
| Adults, New Zealand (Vannoort 1995) | 150 | — |
| Adults, Spain (Urieta 1996) | 286 | — |
| Adults, Japan (Mohri 1990) | 182 | — |
| Children 1–4 yr, Canada (Dabeka 1993) | 14.9 | 11.4–18.1 |
| Children 5–11 yr, Canada (Dabeka 1993) | 29.9 | 25.5–39.7 |
| Children 6–11 mo, United States (Tao and Bolger 1998) | 2.15 | — |
| Children 2 yr, United States | 23.4 | — |
| Children 6 yr, United States | 20.3 | — |
| Children 10 yr, United States | 13.3 | — |
Inorganic-arsenic share of food and water intake (Section 5.5):
| Source | Estimated daily intake of inorganic arsenic |
|---|---|
| Food (assuming 25% of 42 µg/day total arsenic (As) is inorganic) — adults | 10.5 µg/day |
| Drinking water (assuming average level <5 µg/L) — adults | <7.5 µg/day |
| Food (assuming 25% of 14.9 µg/day) — children 1–4 yr | 3.7 µg/day |
| Drinking water (0.7 L/day at <5 µg/L) — children 1–4 yr | <3.5 µg/day |
EPA-approved analytical methods for arsenic in drinking water (Table 2, p. 9):
| Methodology | Reference method | MDL (µg/L) |
|---|---|---|
| Inductively coupled plasma mass spectroscopy (ICP-MS) | EPA 200.8 | 1.4 |
| ICP-MS with selective-ion monitoring | (modification) | 0.1 |
| Stabilized temperature platform graphite furnace AAS (STP-GFAA) | EPA 200.9 | 0.5 |
| Graphite furnace atomic absorption (GFAA) | 3113B (SM) | 1 |
| GFAA | D-2972-93C (ASTM) | 5 |
| Gaseous hydride atomic absorption (GHAA) | 3114B (SM) | 0.5 |
| GHAA | D-2972-93B (ASTM) | 1 |
| EPA 1632 GHAA speciation method | EPA 1632 | 0.002 |
| Practical quantitation limit (PQL) for all EPA-approved methods | — | 3 |
Treatment performance (Section 7.1):
| Technology | Achievable finished-water arsenic |
|---|---|
| Coagulation/filtration with oxidation pretreatment and ion-exchange polishing | 0.003–0.005 mg/L |
| Lime softening | 0.001–0.003 mg/L |
| Activated alumina, pilot plant | <0.01 mg/L; EPA-identified 95% removal as best available technology |
| Ion exchange with oxidation pretreatment | As low as 0.003 mg/L; lab columns to 0.002 mg/L from 0.021 mg/L influent (Clifford 1999) |
| Reverse osmosis | Up to 85% removal of total arsenic |
| Iron oxide-coated sand and granular ferric hydroxide adsorption | Below 0.005 mg/L |
Health-effect anchoring values (Sections 9.1, 9.3):
| Parameter | Value |
|---|---|
| Acute lethal dose range, common arsenic compounds | 1.5 mg/kg bw (As₂O₃) to 500 mg/kg bw (DMAⱽ) (Buchet and Lauwerys 1982) |
| Acute toxicity threshold from well water | Symptoms reported at 1.2 and 21.0 mg/L (Feinglass 1973; Wagner 1979) |
| Dermal lesions threshold (palmoplantar hyperkeratosis, Mee’s lines), 70-kg adult | 5–15 years at ~700 µg/day, or 6 mo–3 yr at ~2,800 µg/day (US EPA 2001a) |
| Half-life of inorganic arsenic in humans | 2–40 days (Pomroy 1980) |
| Relative toxicity order of arsenic species (human hepatocytes, Petrick 2000) | MMAᴵᴵᴵ > arsenite (As(III)) > arsenate (As(V)) > MMAⱽ = DMAⱽ |
| Threshold blood level for teratogenesis (As(III) in pregnant hamsters, Hanlon and Ferm 1986a) | 4.3 µmol/kg |
Southwestern Taiwan cohort (Section 9.1, Chen et al. 1985, 1986, 1992; Wu et al. 1989; Tseng 1977):
| Parameter | Value |
|---|---|
| Total study population (Tseng 1977) | 40,421 |
| Stratification | Low <0.01–0.29 mg/L; medium 0.30–0.59 mg/L; high ≥0.60 mg/L; villages with low/high arsenic well water |
| Population used in 1992 cancer-potency-index re-analysis (Chen 1992) | Stratified into four exposure groups; 13 villages with median <0.10 mg/L, 8 villages 0.10–0.29, 15 villages 0.30–0.59, 6 villages ≥0.60 mg/L |
| Standardized mortality ratios (SMRs), Wu 1989, males / females (bladder, kidney, lung, skin, liver, colon) | Males: 1100, 772, 534, 320, 170, 160; Females: 2009, 1119, 652, 413, 229, 168 |
| Case-control odds ratios, Chen 1986 (40+ year artesian-well exposure, bladder/lung/liver cancer vs never-used controls) | 3.90 / 3.39 / 2.67 |
| Reference high-exposure range | 350 to 1140 µg/L in drinking water |
Antofagasta, Chile cohort (Section 9.1, Zaldívar 1980; Zaldívar and Ghai 1980):
| Parameter | Value |
|---|---|
| Pre-1972 mean arsenic concentration in water | 0.6 mg/L |
| Post-treatment plant installation (1972) mean arsenic concentration | 0.08 mg/L |
| Health effects observed in children under 16 | Leukomelanoderma, hyperkeratosis, respiratory disease, cardiovascular disease, peripheral vascular disorders, Raynaud’s, acrocyanosis, digestive system effects |
US studies cited as not finding clear associations at lower exposures (Section 9.1):
| Study | Population / exposure | Finding |
|---|---|---|
| Steinmaus et al. 2003 | 181 cases / 328 controls, 7 western US counties, 0 to >120 µg/L | No bladder cancer increase at intakes >80 µg/day (OR 0.94, 95% CI 0.56–1.57); smokers ≥80 µg/day, 40-yr lag: OR 3.67 (1.43–9.42) |
| Lamm et al. 2004 | 2.5 million white males, 1950–1979, 3–60 µg/L, 133 counties, 26 states | No arsenic-related increase in bladder cancer mortality; 65% of counties / 82% of population exposed at 3–5 µg/L |
| US EPA and AwwaRF 2004 | 1.5 million people, 32 counties, 11 states, ≥10 µg/L during 1950–1999 | No associations observed for bladder or lung cancer incidence or mortality |
Methods (brief)
This is a federal-provincial-territorial guideline technical document, not a primary research study. The document is the May 2006 update of the Health Canada arsenic guideline, replacing prior guideline technical documents (the 1989 25 µg/L guideline was lowered to 10 µg/L following review of southwestern Taiwan internal-organ cancer evidence, US EPA 2001 review, and US NRC 1999 and 2001 reviews). The document was prepared by the Water Quality and Health Bureau, Healthy Environments and Consumer Safety Branch, Health Canada, and adopted by the Federal-Provincial-Territorial Committee on Drinking Water.
Risk-assessment derivation: Health Canada (2005) applied the Poisson-Weibull model recommended by US EPA (2001a) and fit by Morales et al. (2000) to southwestern Taiwan internal-organ cancer data of Chen et al. (1985) and Wu et al. (1989), using an external unexposed comparison population per US NRC (2001) recommendation. The external comparison population was the southwestern Taiwanese rural population rather than the entire Taiwanese population, to reduce bias from urban–rural differences. Assumptions followed US EPA (2001a): choice of risk metric, 1% extra-risk benchmark response, conversion factor from southwestern Taiwanese to Canadian drinking-water consumption and body weight. The most sensitive endpoint for males and females was lung cancer (3.85 × 10⁻⁵ at 1 µg/L); the lower bound of the unit risk range was liver cancer (3.06 × 10⁻⁶). The unit risk was multiplied by drinking-water arsenic concentrations to produce lifetime cancer risk estimates at 0.3, 5, 10, and 25 µg/L (Table 1).
The MAC was set by considering treatment achievability and the PQL alongside the health-based “essentially negligible” target concentration. The 0.3 µg/L health-based target falls within the 10⁻⁶ to 10⁻⁵ “essentially negligible” range Health Canada applies to carcinogens. The 10 µg/L MAC is acknowledged as a risk-management decision that exceeds the health-based value because it reflects what municipal- and residential-scale treatment can practically achieve and what laboratories can reliably measure. Cancer risk at the MAC (3.0 × 10⁻⁵ to 3.9 × 10⁻⁴) is therefore higher than the “essentially negligible” range, and the document directs ALARA application below the MAC.
Occurrence data were drawn from provincial and territorial monitoring submissions (Prince Edward Island Department of Fisheries, Aquaculture and Environment 2003; Ministère de l’Environnement du Québec 2003; Ontario Ministry of Environment and Energy 2003; Saskatchewan Department of Environment and Resource Management 2003; Alberta Department of Environment 2003; Nova Scotia Department of the Environment 1998; Newfoundland Department of Environment and Labour 2003) and from published Canadian groundwater studies (Méranger 1984; Boyle 1998).
Analytical-methods review summarized the EPA-approved arsenic-in-water methods and method detection limits. The PQL of 3 µg/L is the value EPA assigned for laboratories’ practical measurement capability under EPA-approved methods (US EPA 1999). EPA Method 1632 was singled out as providing direct GHAA speciation of arsenic, with an MDL of 0.002 µg/L, but is described as requiring a high degree of skill.
Treatment-technology review summarized municipal-scale (coagulation/filtration, lime softening, activated alumina, ion exchange, reverse osmosis, manganese greensand filtration, adsorption/filtration with iron-oxide-coated sand or granular ferric hydroxide, electrodialysis reversal) and residential-scale (reverse osmosis, distillation, adsorption/filtration) options, plus water blending as a non-treatment management approach. The document references NSF/ANSI Standards 53 (Drinking Water Treatment Units — Health Effects), 58 (Reverse Osmosis Drinking Water Treatment Systems) and 62 (Drinking Water Distillation Systems) as the relevant certification standards for residential devices; NSF/ANSI standards test for removal to 10 µg/L, and certified devices are often designed to remove arsenic to well below that concentration.
Toxicology synthesis drew on US EPA 2001a, US NRC 1999 and 2001, ATSDR 2000, WHO 2003, IPCS 2001, Health Canada 1998, IARC and Health Canada (1994) carcinogenicity reviews, the southwestern Taiwan cohort (Tseng 1977, Chen 1985, 1986, 1992; Wu 1989), the Chilean (Antofagasta) cohort (Zaldívar 1980; Borgono and Greiber 1971), Bangladeshi (Smith 2000), Indian (Mandal 1998), Mexican (Cebrian 1983), and US (Steinmaus 2003; Lamm 2004; US EPA and AwwaRF 2004; Aschengrau 1989; Zierler 1988) studies, plus animal studies in rats, mice, hamsters, rabbits and chicks (Carmignani 1985; Yamamoto 1995; Wanibuchi 1996, 1997; Hanlon and Ferm 1985, 1986a, 1986b; Hood and Bishop 1972; Zierler 1988; Ferm and Hanlon 1985; Nemec 1998). Genotoxicity, mode-of-action, and relative-toxicity-of-species data (Aposhian 2000; Petrick 2000; Styblo 2000; Mass 2001) were reviewed. Although the document notes recent evidence that MMAᴵᴵᴵ may be more toxic than inorganic species, the Panel concluded the mode-of-action evidence was not strong enough to justify a non-linear quantitative risk assessment model.
Implications
- Reference value: Health Canada’s 2006 MAC of 10 µg/L (0.010 mg/L) for total arsenic in drinking water is a risk-management decision based on treatment achievability and the practical quantitation limit, not on the health-based “essentially negligible” target of 0.3 µg/L. Lifetime cancer risk at the MAC is estimated at 3.0 × 10⁻⁵ to 3.9 × 10⁻⁴, above the 10⁻⁶ to 10⁻⁵ “essentially negligible” range. The Health Canada derivation uses the Morales et al. 2000 Poisson-Weibull dose-response fit to the southwestern Taiwan internal-organ cancer data of Chen et al. 1985 and Wu et al. 1989, per US EPA 2001a’s recommendation. The 10 µg/L MAC is numerically the same as the US EPA 10 µg/L MCL (see EPA — Maximum Contaminant Level for Arsenic in Drinking Water) and the WHO 10 µg/L provisional guideline, but the underlying derivations of those values are not described in this document and should not be presumed identical.
- Speciation discipline: the MAC is set on total arsenic, not inorganic arsenic, despite the document explicitly framing carcinogenic risk on inorganic forms and noting that drinking water arsenic is essentially all inorganic per the US NRC (1999) review. The total-arsenic basis simplifies compliance monitoring; speciation is described as available (EPA Method 1632, HPLC-GHAA, HPLC-ICP-MS) but not required for compliance.
- ALARA framing: the document explicitly directs that arsenic levels in drinking water should be maintained as low as reasonably achievable below the MAC. Residential-scale certified treatment devices reduce arsenic to well below 10 µg/L, and combined-system designs can achieve below 5 µg/L.
- Occurrence context: provincial and territorial monitoring across 1976–2002 indicates Canadian drinking-water arsenic is generally well below the MAC (>97–99% of samples below 10 µg/L in most provinces’ aggregate data), with elevated levels concentrated in well water in areas of natural geological sources (Nova Scotia, Newfoundland, Saskatchewan, Alberta, British Columbia, parts of Ontario). Maximum observed levels reach 105 µg/L (Saskatchewan), 580 µg/L (Bowen Island, BC), 368 µg/L (Newfoundland school wells), 288 µg/L (Newfoundland public wells), and 1000 µg/L (Alberta).
- Dietary context: drinking water is not the major source of arsenic exposure for most Canadians; food is the primary route, principally seafood (78.9% of dietary arsenic intake in a US survey; 94% of total arsenic intake in the 1997 UK MAFF total diet study). However, the inorganic-arsenic share is higher in drinking water than in seafood (where the dominant species is arsenobetaine), so the inorganic-arsenic contribution from drinking water can rival that from food.
- Subgroup framing: Health Canada explicitly states that subpopulations (children, pregnant women) are not at greater risk of developing health effects from arsenic exposure than the general population in the 2006 derivation (Sections 2.1, 3.0). The document references the US NRC conclusion that “there was insufficient scientific information to permit separate cancer risk estimates for potential subpopulations such as pregnant women, lactating women and children” (US EPA 2001a, cited Section 9.1).
Related evidence
- Arsenic
- Arsenic, Inorganic
- Arsenic, Total
- Water
- EFSA — Arsenic in Food (2009), No-PTWI Position
- JECFA inorganic arsenic BMDL₀.₅ (lower-limit benchmark dose)
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