Health And Environmental Effects of
Trace Elements in Mining Waste
We have received many requests for information from residents regarding the human health effects of the proposed mine. At the August 19, Information Session in Sherbrooke, we heard accounts from Harry Kelly regarding some of the effects of dust from the mine on residents within the footprint of the mine. Dust is supposed to be supressed or controlled as stipulated in the Industrial Permit granted Atlantic NS Mining Corp. for the Touquoy mine. This permit is governed by the Department of the Environment, issuer of the permit. Besides the local residents airways, who is monitoring dust levels?
If the Cochrane Hill Project is approved how rigorous, will the monitoring program for surface and groundwater be? In addition to the proponents monitoring requirements, is there a case for requesting the regulators designate an independent program/entity aimed at monitoring these and other water quality parameters to ensure transparency, increased sample frequency and timely reporting for non-compliance? I understand, The Eastern Shore Forestry Watch conducts a similar program for the Touquoy mine.
Thanks to John Perkins of SuNNS, for providing this reference “HEALTH & ENVIRONMENTAL EFFECTS OF TRACE ELEMENTS IN METAL-MINING WASTES “. The Fate, Ecotoxicity and Human Health effects of arsenic, cadmium, cyanide, lead, copper, mercury and zinc are summarized below. A more detailed copy of the information may be downloaded here. Source: CP2 – The Center for Science in Public Participation, an American based organization. Note, the reference refers to American standards, see end of the blog for links to Canadian standards. For human effects look for the MCL level and for aquatic species the CMC level.
Note that Ann Masest, the consultant SMRA has engaged to review the Environmental Impact Statement has expertise in the area of mine waste fate and transport.
TERMS USED IN THE REFERENCE
Fate: Refers to the solubility, persistence and bioaccumlation of the element in the environment.
Ecotoxicity: Refers to the nature, effects, and interactions of substances that are harmful to the environment.
Persistence: The length of time a compound stays in the environment.
Bioaccumulation: The extent to which substances increase in concentration in contaminated air, water or food because the substances are very slowly metabolized or excreted.
Solubility: The amount of mass of a compound that will dissolve in a unit volume of solution.
MRL: Minimal Risk Level – an estimate of the daily human exposure to a hazardous substance that is likely to be without an appreciable risk of adverse (noncarcinogenic) health effects over a specified duration of exposure.
MCL: Maximum contaminant level – an enforceable EPA standard for drinking water contamination.
CCC: Criterion Continuous Concentration – an estimate of the highest concentration of a material in surface water to which an aquatic community can be exposed indefinitely without resulting in an unacceptable effect.
CMC: Criterion Maximum Concentration – an estimate of the highest concentration of a material in surface water to which an aquatic community can be exposed briefly without resulting in an unacceptable effect.
LD: Lethal Dose; LD50/Lethal Dose is the dose of a toxicant or microbe that will kill 50% of the test organisms within a designated period. The lower the LD50, the more toxic the compound.
LOAEL: Lowest-observed-adverse effect level.
NIWQP: National Irrigation Water Quality Program Information Report No. 3 (U.S. Department of the Interior)
NRWQC: National Recommended Water Quality Criteria
SMCL: Secondary maximum contaminant level – non enforced EPA guidelines to manage water for aesthetic consideration
Arsenic – As
Fate: • Persistence: cannot be destroyed; can only change its form • Solubility: many As compounds dissolve in water; native forms are not very important in natural systems and seldom exist in the environment; they are always associated with metals (Fe) or sulfides (S), etc. As can be dissolved in oxidizing acids. • Bioaccumulation: by fish and shellfish
Ecotoxicity: Terrestrial flora and fauna, birds, and freshwater biota usually contain < 1 mg/As/kg by wet weight (NIWQP); however, much higher concentrations, if contaminated. Freshwater NRWQC – CCC: 150 μg/L; CMC: 340 μg/L. Toxicity in water is determined by water temperature, pH, organic content, phosphate concentration, suspended soils, presence of oxidants, and speciation. As and Se have been found to have an antagonistic interaction in several animal species. Freshwater LOAEL (As-V): 850 μg/L for acute exposure (NIWQP).
Human Health Effects: Health organizations advise treating all As compounds as highly toxic. MRLs have been defined as 0.005 mg/kg/day for Provisional Oral Acute (14 days or less), and 0.0003 mg/kg/day for chronic (365 days or less)1. High levels: Death – as little as 70-200 mg of As(III) ingested by an adult may be lethal; inorganic As can increase risk of cancers (lung, skin, bladder, liver, kidney, prostate); breathing inorganic As causes sore throat, irritated lungs. Lower levels: pins and needles in hands/feet; damage to blood vessels, nausea, vomiting; darkening of skin, appearance of ‘corns’ or ‘warts’ on palms, soles, torso; skin contact causes redness or swelling As(V) is a carcinogen and skin is a possible absorption route. Inhalation/ingestion causes lung/liver, kidney, bladder cancer.
Cadmium – Cd
Fate: • Persistence: Does not break down in the environment, but can change form. Solubility: Varies, depending upon form. Cd carbonate is insoluble, whereas Cd nitrate is soluble. Oxides and sulfides are relatively insoluble; chlorides and sulfates salts are soluble.
Bioaccumulation: Fish, plants, and animals uptake Cd from environment. Bioaccumulation factors vary; rainbow trout BCF=33; mosquito fish BCF = 2213.
Ecotoxicity: Animals given Cd in food or water develop high blood pressure, iron-poor blood, liver disease, nerve/brain damage. Affects birth weight and skeleton in developing animals. Cadmium is toxic to aquatic organisms at relatively low levels. Freshwater NRWQC – CCC: 0.25 μg/L; CMC: 2.0 μg/L Toxicity Thresholds (NIWQP) Cd and its solutions are extremely toxic.
Human Health Effects: The Oral Chronic Minimal risk level (MRL) is 0.0002 mg/kg/day. 4 mg of cadmium inhaled can be fatal. Ingestion of more than 100 mg of soluble Cd salt may be lethal. Cd stays in the body a very long time and bioaccumulates from many years of exposure to low levels. The general population can be exposed to Cd in the workplace where Cd products are made, by breathing cigarette smoke, and Cd-contaminated air near the burning of fossil fuels and municipal waste, and also eating Cd-contaminated foods. People who work with lead and lead ores may be exposed to Cd vapors. OSHA PEL is 0.005 mg/m3 for Cd dust or fume. Lung inflammation results from inhaling air containing 0.5-2.5 mg/m3 of Cd dust and breathing high levels causes death. Cd is also a severe lung and gastrointestinal irritant. It causes kidney disease, fragile bones, irritates the digestive tract, and causes vomiting, and diarrhea. Long-term exposure to lower levels in air, food, and water leads to buildup of Cd in kidneys, causing kidney and liver damage, anemia and loss of the sense of smell. 1 Minimal Risk Levels for Hazardous Sub
Copper – Cu
Fate: • Persistence: Cu+2 free ion decreases as CuCO3, CuOH+, and Cu2(OH)2 +2 increase. • Solubility: Solubility depends upon the compound; acidic waters increase solubility. • Bioaccumulation: Cu does not appear to bioaccumulate except in chicken livers (NIWQP, p. 51).
Ecotoxicity: High concentrations of Cu in rivers resulting from metal extraction adversely affect fisheries. Generally more toxic to aquatic organisms than to birds or mammals. Mixtures of Cu and Zinc are known to be additive or synergistic in toxicity to many aquatic organisms (NIWQP, p. 52). High levels of Cu are toxic to soil organisms. • Freshwater NRWQC – CCC: 9.0 μg/L; CMC: 13 μg/L • The presence of zinc and copper together is known to cause increased toxicity to aquatic organisms Toxicity Thresholds (NIWQP) • Plants (mg/kg dw): >20 • Fish, whole body (mg/kg dw): 13.3 • Birds, liver (mg/kg dw): >540
Human Health Effects: Metallic Cu has little toxicity, but Cu’s soluble salts are poisonous. Low levels of Cu are essential for maintaining good health (RDA for adults = 900 g/day); high levels can cause harmful effects such as skin allergies and irritation of the nose, mouth, eyes, nausea, diarrhea, vomiting, stomach cramps. The Minimum Risk Level (MRL) of 0.02 mg/kg/day has been derived for acute (duration 1-14 days) oral exposure to Cu.1 Short periods of exposure can result in gastrointestinal disturbance; long periods can result in kidney/liver damage. It may decrease fertility in adults. Breathing Cu-containing dust or skin contact (in mining Cu or processing ore) can cause death and liver/kidney disease (OSHA exposure limit is 1 mg/m3 for Cu dust and 0.1 mg.m3 for Cu fume). Exposure to Cu in tap water (from Cu pipes and brass faucets) can be reduced by running water 15-30 seconds before use.
Fate: • Persistence: Most persistent in groundwater, and at higher pH. Cyanate (CNO- ) and Thiocyanate (SCN- ) compounds are more persistent than CN- , and do have significant toxicity • Solubility: varies with compound; cyanohydrins and highly soluble; organic cyanides are slightly soluble; hydrogen cyanide is soluble; Ni-, Cu-, Ag-, Zn- and Fe- cyanides are relatively insoluble. • Bioaccumulation: Does not bioaccumulate in fish
Ecotoxicity: Freshwater NRWQC – CCC: 5.2 μg/L; CMC: 22 μg/L
Human Health Effects: The Minimum Risk Level (MRL) derived for sodium CN is 0.05 mg/kg/day for intermediate duration (15-364 days) for oral exposure.1 Oral lethal dose of KCN for an adult is 200 mg; airborne concentrations of 270 ppm is immediately fatal and a concentration of 110 ppm for half an hour is lifethreatening. In addition, short time high level exposures result in brain and heart damage and can cause coma and death. Long term exposure to lower levels results in heart pains, breathing difficulties, vomiting, blood changes, headaches and thyroid gland enlargement. Salts can be rapidly adsorbed by inhalation; ingestion; through the skin. High blood cyanide levels results in weakness of fingers and toes, difficulty walking, dimness of vision, deafness and decreased thyroid gland function.
Lead – Pb
Fate: • Persistence: Does not break down; compounds are changed by sunlight, air, and water • Solubility: pure Pb has a low solubility in water (least soluble at pH 8-10); compounds vary in solubility; dissolves more easily at low pH • Bioaccumulation: in plants and animals (does not accumulate in fish, but does in some shellfish, e.g., mussels; and mammal bones) Ecotoxicity: Toxic to all aquatic organisms; as dissolved oxygen levels decrease, Pb increases in toxicity to fish. Toxicity increases if water is acidic or ‘soft.’ • Freshwater NRWQC – CCC: 2.5 μg/L; CMC: 65 μg/L Human Health Effects: While no acute intermediate or chronic MRLs1 have been derived for any route of exposure, ATSDR reports a framework to guide public health assessment decisions at lead sites (see Appendix D-1 Toxicological Profile for Lead, http://www.atsdr.cdc.gov/tp13.pdf) CDC defines elevated level for children as 10 μg/dL (ppb) in the blood; greater than 125 μg/dL, death results. When blood levels in children is greater than 90 μg/dL, acute Pb toxicity occurs with ataxia, coma, and convulsions as symptoms. For adults, it is estimated that death occurs 1-2 days after ingestion of 10-30 g of a lead salt.2 Pregnant women exposed to Pb can have premature births and smaller babies; infants and children are particularly sensitive to chronic effects of Pb, e.g., decreased mental ability, delays in physical/mental development; attention span deficits, learning disabilities. Chronic effects include stroke, kidney disease, kidney and brain damage, high blood pressure, nervous/reproductive system damage, decreased reaction time, weakness in fingers, wrists, ankles, and probable cancer (if lifetime exposure). Repeated exposure causes Pb to accumulate in human body. OSHA PEL = 0.05 mg/m3 . EPA lists lead and inorganic compounds of lead as “B2” – a probable human carcinogen. Occupational exposure occurs mainly from breathing dust and fumes, with workers in smelting/refining, battery manufacture/reclamation at higher risk. 1 Toxicological Profile for Lead, US Department of Health and Human
Mercury – Hg
Fate: Hg undergoes biogeochemical cycling: it degasses from soils and surface waters, is transported through the atmosphere, deposits on land and surface waters, is sorbed into soil and sediment particulates, and degasses, etc. • Persistence: can change form, cannot be destroyed • Solubility: Cinnabar (HgS) is insoluble (and resists weathering); liquid Hg is slightly soluble in water. • Bioaccumulation: Hg Methylation forms CH3Hg+ which is easily absorbed by organisms and biomagnifies from the bottom to the top of the food chain; concentrates in muscle and tissue of fish and other wildlife, which bioaccumulate it. CH3Hg+ generally increases by a factor of ten or less with each step up the food chain. Bioaccumulation factors of 63,000 for freshwater fish, 10,000 for salt water fish, 100,000 for marine invertebrates, and 1000 for freshwater and marine plants have been found.
Ecotoxicity: 0.012 mg/L instream concentration results in chronic effects to aquatic life; concentrations of Hg(0), Hg(II), or CH3Hg+ may be low in streams, but due to bioaccumulation and biomagnification, CH3Hg+ in fish may be toxic to humans and fish-eating wildlife (such as bald eagles). When Hg and Se interact in various species of wildlife, both antagonistic and synergistic effects have been observed. • Hg Freshwater NRWQC – CCC: 0.77 μg/L; CMC: 1.4 μg/L Toxicity Thresholds (NIWQP) • Fish (cold-water species) (mg/kg ww): 1.0 • Birds, diet (mallards) (mg/kg bw/day: 0.064; loons: 0.3 Human
Health Effects: CH3Hg+ is a neurotoxin and is the most toxic form; consuming Hg contaminated water/wildlife and fish can result in kidney, brain, cardiovascular damage/death. People uptake Hg as CH3Hg+ or breathe vapors emitted from metallic Hg, dental amalgams, and ambient air (OSHA PEL=0.1 mg/m3 ). Prenatal effects occur at levels 5-10 times lower than that of adults. The MRL1 for Hg, for chronic inhalation is 0.0002 mg/m3 (or 0.2 μg/m3 ). The chronic oral MRL for methyl mercury for a 70 kg adult is 0.0003 mg/kg/day.2
Zinc – Zn
Fate: • Persistence: Cannot be broken down • Solubility: Zn metal is not soluble; some compounds of Zn are water soluble • Bioaccumulation: varies greatly; BCF for insects ~ 107-1,130; BCF fish ~51-432
Ecotoxicity Mixtures of Cu and Zinc are known to be additive or synergistic in toxicity to many aquatic organisms (NIWQP, p. 52, 190). Other metals that are additive to zinc in toxicity are lead and nickel; cadmium is known to be antagonistic to zinc (NIWQP, p. 190). Zn toxicity in water is affected by hardness, pH, temperature, dissolved oxygen, and alkalinity. Dissolved Zn is toxic to fish. • Freshwater NRWQC – CCC: 120 μg/L; CMC: 120 μg/L Toxicity Thresholds (NIWQP – mg/kg dw) • Plants: > 300; oak/maple seedlings died when Zn soil levels were > 100 mg/kg dw • Fish, white sucker muscle tissue: 20 • Birds, liver/kidney: > 2,100 • Mammals, Kidney: >274; Liver: >465
Human Health Effects: Low levels of Zn are essential for maintaining good health: RDA for adults = 8 mg/day (females); 11 mg/day (males); too little and too much Zn are harmful to health. Inhalation or contact with decomposition products, vapors, or substance may cause death or severe injury. Signs of deficiency include growth retardation, hair loss, diarrhea, delayed sexual maturation, eye and skin lesions (slow wound healing), damaged immune system, and loss of appetite. Zn toxicity has acute and chronic forms: 150-450 mg have been associated with low copper status, altered iron function, reduced immune function. Eating large amounts, even for a short time, causes stomach cramps, nausea, and vomiting; chronic use can cause anemia, pancreas damage, and lower levels of high density lipoprotein cholesterol (the good form of cholesterol). Breathing zinc dust or fumes causes ‘metal fume fever’; OSHA PEL for Zinc chloride fumes = 1 mg/m3 ; PEL for Zinc oxide fumes=5 mg/m3 . An MRL of 0.3 mg/kg/day (Oral, Intermediate duration (15-364 days) and 0.3 mg/kg/day, chronic (365 days or more) has been derived.
The guidelines noted in the reference above are EPA standards and not the Canadian standards. In Canada our guidelines are governed by two organizations, the first CCME: Canadian Council for the Ministers of the Environment. These guidelines govern everything except drinking water for humans and recreational activity in water, which are governed by Health Canada. The levels of these elements will be important to monitor not only for humans but also for, aquatic species, flora and fauna, and for the safety of recreational activities that take place within the impacted water bodies for the project.
Guidelines for Canadian Drinking Water Quality
The Guidelines for Canadian Drinking Water Quality are published by Health Canada on behalf of the Federal-Provincial-Territorial Committee on Drinking Water (CDW).
Guidelines for Canadian Recreational Water Quality
Regulations on recreational water quality are a provincial and territorial responsibility. Health Canada worked with officials in these areas to develop and publish national guidelines for recreational water quality.
- Download Chapter PDF Water Quality Guidelines for the Protection of Aquatic Life Freshwater, Marine
- Download Chapter PDF Sediment Quality Guidelines for the Protection of Aquatic Life Freshwater and Marine ISQG/PEL
- Download Chapter PDF Soil Quality Guidelines for the Protection of Environmental and Human Health Agricultural, Residential/Parkland, Commercial, Industrial
- Download Chapter PDF Tissue Residue Quality Guidelines for the Protection of Wildlife Consumer of Aquatic Biota