Page 2: Sixth Report on Human Biomonitoring of Environmental Chemicals in Canada

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8 Summaries and results for metals and trace elements

8.1 Lead

Lead (CASRN 7439-92-1) is a naturally occurring element. It is a base metal and can exist in various oxidation states in both inorganic and organic forms (ATSDR, 2020). Elemental lead is an inorganic form, while organic lead compounds include dialkyl, trialkyl and tetra-alkyl lead.

Lead is found in bedrock, soils, sediments, surface water, groundwater and sea water (HC, 2013a). It enters the environment from a variety of natural and anthropogenic sources. Natural processes include soil weathering, erosion and volcanic activity (ATSDR, 2020; IARC, 2006). Lead released from industrial emissions can be a major source of environmental contamination, especially near point sources, such as smelters or refineries (ATSDR, 2020). Historical use of leaded motor fuels has contributed to the ubiquitous distribution of lead throughout the world (WHO, 2000).

In North America, tetraethyl and tetramethyl lead were added to motor vehicle fuels as an anti-knock agent until the 1990s. Today in Canada, the addition of lead to gasoline is prohibited, with the exception of fuels for piston engine aircraft and racing fuels for competition vehicles (Canada, 1990; HC, 2013a). Lead is currently used in the refining and manufacturing of products such as lead acid automotive batteries, lead shot and fishing weights, sheet lead, lead solder, some brass and bronze products, and some ceramic glazes (ATSDR, 2020; WHO, 2000). Other uses of lead include dyes in paints and pigments. It is also used in scientific equipment, as a stabilizer in plastics, in military equipment and ammunition, and in radiation detection and medical equipment for radiation shielding (ATSDR, 2020; WHO, 2000). Lead is also used in the manufacturing of cable sheathing, circuit boards, chemical baths and storage vessel linings, chemical transmission pipes, electrical components and polyvinyl chloride (HC, 2013a).

Everyone is exposed to trace amounts of lead through food, drinking water, soil, household dust, air and some consumer products. However, lead exposure in Canada has decreased by approximately 80% over the past 40 years (ECCC, 2020). This decrease is largely attributed to the phase-out of leaded gasoline, restrictions on the use of lead in consumer paints and other coatings on children's products, and the elimination of lead solder in food cans. Today, the main route of exposure for the general adult population is ingestion via food and drinking water (ATSDR, 2020; HC, 2013a). For infants and children, the primary sources of exposure are food, drinking water, and non-food items containing lead, such as house dust, paint, soil and consumer products (HC, 2013a). Lead can enter the water supply from lead service lines in older homes, brass plumbing fittings that contain lead, or lead solder in the plumbing in homes (HC, 2016). Other potential sources of exposure include: costume jewellery, art supplies, leaded crystal and glazes on ceramics and pottery; having a hobby (or living with someone who has) that requires the use of lead or lead solder, such as refinishing furniture or making stained glass, ceramic glazing, lead shot or lead fishing weights; living near airports with piston aircraft activity; and smoking (HC, 2013b). The Canadian House Dust Study reported that lead is enriched in house dust compared with the natural geochemical background as a result of the use of lead in consumer products, paints and building materials as well as infiltration from outdoor sources (Rasmussen et al., 2013).

Approximately 3% to 10% of ingested lead is absorbed into blood in adults; the amount absorbed can increase to up to 40% to 50% in children (HC, 2013a). Nutritional calcium and iron deficiencies in children appear to increase lead absorption and decrease lead excretion (HC, 2013a). Once absorbed by the human body, lead circulates in the bloodstream, where it accumulates in tissues, particularly bone, and is excreted from the body. Some lead may also be sequestered in soft tissues, such as the liver, kidneys and lungs. Bones account for approximately 70% of the total body burden of lead in children and more than 90% of the total body burden in adults (EPA, 2006). Lead stored in bone can be remobilized and released back into circulating blood. Pregnancy, lactation, menopause, andropause, post-menopause, extended bed rest, hyperparathyroidism and osteoporosis are all conditions that can increase remobilization of lead from bone, increasing blood lead levels (HC, 2013a).

During pregnancy, lead stored in maternal bone becomes a source of exposure for both fetus and mother (Rothenberg et al., 2000). Lead can also be present in breast milk and transferred from lactating mothers to infants (ATSDR, 2020; EPA, 2006). The half-life for lead in blood is approximately 30 days, whereas the half-life for lead accumulated in the body, such as in bone, is in the range of 10 to 30 years (ATSDR, 2020; HC, 2009a; 2013a). Excretion of absorbed lead occurs primarily through urine and feces, regardless of the route of exposure (ATSDR, 2020). Blood lead is the preferred indicator of human exposure to lead, although other matrices — such as urine, bone and teeth — also have been used (ATSDR, 2020; CDC, 2009). Lead is considered a cumulative general toxicant, with developing fetuses, infants, toddlers and children being most susceptible and vulnerable to adverse health effects (WHO, 2011). Following acute exposure, a variety of metabolic processes may be affected. Very high exposure may result in vomiting, diarrhea, convulsions, coma and death. Cases of lead poisoning are rare in Canada (HC, 2009a).

Chronic low-level exposure may affect both the central and peripheral nervous systems; however, the symptoms of relatively low exposure levels are often not apparent (ATSDR, 2020; HC, 2013a). Chronic low-level exposure to lead has also been associated with developmental neurotoxicity, neurodegenerative effects, cardiovascular disease, decreased renal functioning, reproductive problems and other health responses (ATSDR, 2020; Bushnik et al., 2014; HC, 2013a; Lanphear et al., 2018). Cognitive and neurobehavioural effects have been recognized as major concerns for exposed children. In infants and children, exposure to lead is most strongly associated with neurodevelopmental effects, specifically the reduction of intelligence quotient (IQ) (Lanphear et al., 2005) and an increased risk of attention-related behaviours (HC, 2013a). Based on available data, no threshold has yet been identified for the effects of lead exposure on cognitive function and neurobehavioural development, meaning that no safe level of exposure is known to exist (CDC, 2012; EPA, 2006; HC, 2013a). Developmental neurotoxicity has been associated with the lowest levels of lead exposure measured to date, although there is uncertainty associated with effects observed at these levels (HC, 2013a). The International Agency for Research on Cancer classifies inorganic lead compounds as Group 2A, probably carcinogenic to humans (IARC 2006).

Lead is listed on Schedule 1, List of Toxic Substances, under the Canadian Environmental Protection Act, 1999 (CEPA 1999). The act allows the federal government to control the importation, manufacture, distribution and use of lead and lead compounds in Canada (Canada, 1999; HC, 2009a). Lead is subject to numerous federal risk management initiatives in Canada directed toward industrial releases, consumer products, cosmetics, drinking water, food, natural health products, therapeutic products, tobacco and environmental media, including household dust, soil and air. CEPA 1999 prohibits the addition of lead in gasoline and controls its release from secondary lead smelters, steel manufacturing and mining effluents (ECCC, 2018). The use of lead in toys, children's jewellery, clothing and accessories, and other products intended for children — along with consumer paints and surface coatings, glazed ceramics and glassware for food storage, and other consumer products that represent a potential risk of lead exposure — is limited under the Canada Consumer Product Safety Act and its associated regulations (Canada, 2010a; Canada, 2010b; HC, 2013a). These include the Children's Jewellery Regulations, which establish a new guideline limit for lead in children's jewellery (Canada, 2016a). In addition, the Consumer Products Containing Lead Regulations limit the total lead content in an expanded scope of consumer products intended for use by a child or an adult in caring for a child (Canada, 2016b). Lead and its compounds are on the List of Ingredients that are Prohibited for Use in Cosmetic Products (HC, 2019b).

On the basis of treatment achievability, Health Canada, in collaboration with the Federal-Provincial-Territorial Committee on Drinking Water, developed a guideline for Canadian drinking water quality that establishes the maximum acceptable concentration for lead (HC, 2019a). Health Canada has also published guidance on controlling corrosion in drinking water distribution systems to help control the leaching of metals, including lead, from system materials and components (HC, 2009b). The concentration of lead in specific foods is managed by Health Canada under the Food and Drug Regulations (Canada, 1978); the existing maximum levels for lead in foods are found in the List of Contaminants and Other Adulterating Substances in Foods. Health Canada has updated the maximum level for lead in fruit juice, fruit nectar and water in sealed containers (HC, 2020b), and for lead in concentrated and ready-to-serve infant formula (HC, 2020d). Maximum levels for other foods and beverages are scheduled for review and update. These regulatory updates are among several Health Canada activities that are underway to ensure that dietary exposure to lead is as low as is reasonably achievable (HC, 2017). Lead is also included in the list of trace elements analyzed as part of Health Canada's ongoing Total Diet Study surveys (HC, 2020a). The food items analyzed represent those that are most typical of the Canadian diet, and the surveys are used to provide dietary exposure estimates for chemicals that Canadians in different age-sex groups are exposed to through the food supply. From 1981 to 2000, Canadians' average dietary exposure to lead decreased approximately eightfold and has remained stable at low levels since that time (HC, 2020c).

In 1994, the Federal-Provincial-Territorial Committee on Environmental and Occupational Health recommended a blood-lead intervention level of 10 µg/dL as guidance for low-level exposure to lead (CEOH, 1994). Scientific assessments indicate that chronic health effects are occurring in children at blood-lead levels below 10 µg/dL, and that there is sufficient evidence that blood-lead levels below 5 µg/dL are associated with adverse health effects (HC, 2013a). Despite some uncertainties, the evidence for an association between neurodevelopmental effects in children and blood-lead levels in the lower range of exposure is of concern. The current guidance for lead in blood (CEOH, 1994) is under review by the federal, provincial and territorial Council of Chief Medical Officers of Health.

Blood-lead levels have been measured in a number of biomonitoring studies conducted in Canada, including the Maternal–Infant Research on Environmental Chemicals study (Arbuckle et al., 2016) and the First Nations Biomonitoring Initiative (AFN, 2013).

Lead was analyzed in the whole blood of Canadian Health Measures Survey (CHMS) participants aged 6–79 in cycle 1 (2007–2009), and aged 3–79 in cycle 2 (2009–2011), cycle 3 (2012–2013), cycle 4 (2014–2015), cycle 5 (2016–2017) and cycle 6 (2018–2019). Data from these cycles are presented in blood as µg/dL. Lead was also analyzed in hair from CHMS participants aged 20–59 in cycle 5.

References

• AFN (Assembly of First Nations) (2013). First Nations Biomonitoring Initiative: National Results (2011). Assembly of First Nations, Ottawa, ON. Retrieved February 2, 2021.
• Arbuckle, T.E., Liang, C.L., Morisset, A.S., Fisher, M., Weiler, H., Cirtiu, C.M., Legrand, M., Davis, K., Ettinger, A.S., Fraser, W.D., et al. (2016). Maternal and fetal exposure to cadmium, lead, manganese and mercury: The MIREC study. Chemosphere, 163, 270–282.
• ATSDR (Agency for Toxic Substances and Disease Registry) (2020). Toxicological Profile for Lead. U.S. Department of Health and Human Services, Atlanta, GA. Retrieved February 22, 2021.
• Bushnik, T., Levallois, P., D'Amour, M., Anderson, T.J., and McAlister, F.A. (2014). Association between blood lead and blood pressure: Results from the Canadian Health Measures Survey (2007 to 2011). Health Reports, 25(7), 12–22.
• Canada (1978). Food and Drug Regulations. C.R.C., c. 870. Retrieved February 3, 2021.
• Canada (1990). Gasoline Regulations. SOR/90-247. Retrieved February 22, 2021.
• Canada (1999). Canadian Environmental Protection Act, 1999. SC 1999, c. 33. Retrieved February 22, 2021.
• Canada (2010a). Canada Consumer Product Safety Act. SC 2010, c. 21. Retrieved February 22, 2021.
• Canada (2010b). Consumer Products Containing Lead (Contact with Mouth) Regulations. SOR/2010-273. Retrieved February 22, 2021.
• Canada (2016a). Children's Jewellery Regulations. SOR/2016-168. Retrieved February 22, 2021.
• Canada (2016b). Consumer Products Containing Lead Regulations. Canada Gazette, Part I: Notices and Proposed Regulations, 150(49). Retrieved February 22, 2021.
• CDC (Centers for Disease Control and Prevention) (2009). Fourth National Report on Human Exposure to Environmental Chemicals. Department of Health and Human Services, Atlanta, GA. Retrieved February 22, 2021.
• CDC (Centers for Disease Control and Prevention) (2012). CDC Response to Advisory Committee on Childhood Lead Poisoning Prevention: Recommendations in "Low level Lead Exposure Harms Children: A Renewed Call of Primary Prevention". Department of Health and Human Services, Atlanta, GA. Retrieved February 22, 2021.
• CEOH (Federal-Provincial Committee on Environmental and Occupational Health) (1994). Update of evidence for low-level effects of lead and blood-lead intervention levels and strategies – final report of the working group. Minister of Health, Ottawa, ON.
• ECCC (Environment and Climate Change Canada) (2018). Toxic substances list: lead. Minister of Environment and Climate Change, Ottawa, ON. Retrieved February 22, 2021.
• ECCC (Environment and Climate Change Canada) (2020). Canadian Environmental Sustainability Indicators: Human exposure to harmful substances. Minister of Environment and Climate Change, Ottawa, ON. Retrieved January 25, 2021.
• EPA (U.S. Environmental Protection Agency) (2006). Air quality criteria for LEAD (Final Report, 2006) – Volume I and II. U.S. Environmental Protection Agency, Washington, DC. Retrieved February 22, 2021.
  
  HC (Health Canada) (2009a). Lead Information Package – Some Commonly Asked Questions About Lead and Human Health. Minister of Health, Ottawa, ON. Retrieved February 22, 2021.
• HC (Health Canada) (2009b). Guidance on Controlling Corrosion in Drinking Water Distribution Systems. Minister of Health, Ottawa, ON. Retrieved February 22, 2021.
• HC (Health Canada) (2013a). Final Human Health State of the Science Report on Lead. Minister of Health, Ottawa, ON. Retrieved February 22, 2021.
• HC (Health Canada) (2013b). It's Your Health: Lead and Human Health. Minister of Health, Ottawa, ON. Retrieved February 22, 2021.
• HC (Health Canada) (2016). Water Talk: Lead in drinking water. Minister of Health, Ottawa, ON. Retrieved February 22, 2021.
• HC (Health Canada) (2017). Notice of Modification to the List of Contaminants and Other Adulterating Substances in Foods to Update the Maximum Levels for Lead in Fruit Juice, Fruit Nectar and Water in Sealed Containers. Minister of Health, Ottawa, ON. Retrieved February 22, 2021.
• HC (Health Canada) (2019a). Guidelines for Canadian Drinking Water Quality: Guideline Technical Document – Lead. Minister of Health, Ottawa, ON. Retrieved February 22, 2021.
• HC (Health Canada) (2019b). List of Ingredients that are Prohibited for Use in Cosmetic Products (Hotlist). Minister of Health, Ottawa, ON. Retrieved February 22, 2021.
• HC (Health Canada) (2020a). Concentration of Contaminants and Other Chemicals in Food Composites. Minister of Health, Ottawa, ON. Retrieved February 22, 2021.
• HC (Health Canada) (2020b). Food Directorate updated approach for managing dietary exposure to lead. Minister of Health, Ottawa, ON. Retrieved February 22, 2021.
• HC (Health Canada) (2020c). Lead. Minister of Health, Ottawa, ON. Retrieved February 22, 2021.
• HC (Health Canada) (2020d). Notice of modification to lower the maximum levels for lead in concentrated infant formula and infant formula when ready-to-serve in the list of contaminants and other adulterating substances in foods. Minister of Health, Ottawa, ON. Retrieved January 25, 2021.
• IARC (International Agency for Research on Cancer) (2006). IARC Monographs on the Evaluation of Carcinogenic Risks to Humans - Volume 87: Inorganic and Organic Lead Compounds. World Health Organization, Lyon. Retrieved February 22, 2021.
• Lanphear, B.P., Hornung, R., Khoury, J., Yolton, K., Baghurst, P., Bellinger, D.C., Canfield, R.L., Dietrich, K.N., Bornschein, R., Greene, T., et al. (2005). Low-level environmental lead exposure and children's intellectual function: An international pooled analysis. Environmental Health Perspectives, 113(7), 894–899.
• Lanphear, B.P., Rauch, S., Auinger, P., Allen, R.W., and Hornung, R.W. (2018). Low-level lead exposure and mortality in US adults: a population-based cohort study. The Lancet, Public Health, 3(4), 177–184.
• Rasmussen, P.E., Levesque, C., Chénier, M., Gardner, H.D., Jones-Otazo, H., and Petrovic, S. (2013). Canadian House Dust Study: Population-based concentrations, loads and loading rates of arsenic, cadmium, chromium, copper, nickel, lead, and zinc inside urban homes. Science of the Total Environment, 443, 520–529.
• Rothenberg, S.J., Khan, F., Manalo, M., Jiang, J., Cuellar, R., Reyes, S., Acosta, S., Jauregui, M., Diaz, M., Sanchez, M., et al. (2000). Maternal bone lead contribution to blood lead during and after pregnancy. Environmental Research, 82(1), 81–90.
• WHO (World Health Organization) (2000). Air quality guidelines for Europe, second edition. WHO, Geneva. Retrieved February 22, 2021.
• WHO (World Health Organization) (2011). Lead in Drinking-water: Background document for development of WHO Guidelines for Drinking-water Quality. WHO, Geneva. Retrieved February 22, 2021.

8.2 Arsenic

Arsenic (CASRN 7440-38-2) is a naturally occurring element. It is classified as a metalloid, exhibiting properties of both a metal and a non-metal. Arsenic is commonly found as an inorganic sulphide complexed with other metals (CCME, 1997). It also forms stable organic compounds in its trivalent (III) and pentavalent (V) states. Common organic arsenic compounds include monomethylarsonic acid (MMA), dimethylarsinic acid (DMA), arsenobetaine and arsenocholine (WHO, 2001).

Arsenic may enter lakes, rivers or groundwater naturally through erosion and weathering of soils, minerals and ores (HC, 2006). Anthropogenic sources of arsenic in the environment include the smelting of metal ores, the use of arsenical pesticides and the burning of fossil fuels (WHO, 2001).

Arsenic is used in the manufacture of transistors, lasers and semiconductors and in the processing of glass, pigments, textiles, paper, metal adhesives, ceramics, wood preservatives, ammunition and explosives. Historical uses include application of lead arsenate as a pesticide in apple orchards and vineyards and arsenic trioxide as an herbicide (ATSDR, 2007; HC, 2006). Chromated copper arsenate has been used as a wood preservative in residential construction projects, such as playground structures and decks; however, it is now approved only for industrial purposes and domestic wood foundations (HC, 2011). In 2004, the wood-treatment industry in the U.S. and Canada began to transition away from chromated copper arsenate for most residential uses. Organic arsenical herbicides are no longer registered for use in Canada (HC, 2019).

The public can be exposed to arsenic through food, drinking water, soil, and ambient air (EC and HC, 1993). Food is the major source of exposure, with total arsenic concentrations being highest in seafood (IARC 2012). Organic forms of arsenic, including arsenobetaine and arsenocholine, make up the majority of arsenic in seafood (Ackley et al., 1999; Leufroy et al., 2011; Ruttens et al., 2012), while in other foods, the proportions of organic and inorganic arsenic forms may vary (Batista et al., 2011; CFIA, 2013; Conklin and Chen, 2012; FDA, 2016; Huang et al., 2012). Exposure may also arise from indoor house dust; levels of arsenic in dust can exceed levels in soil (Rasmussen et al., 2001). Further, exposure to arsenic may be elevated in populations residing in areas where industrial or natural sources occur.

Inorganic and organic arsenic can be absorbed via oral and inhalation routes; arsenic in all its forms is not readily absorbed via skin contact. Absorption of arsenic is much lower for highly insoluble forms of arsenic, such as arsenic sulfide, arsenic triselenide and lead arsenate (ATSDR, 2007). Following absorption, arsenic appears rapidly in blood circulation, where it binds primarily to haemoglobin. Within 24 hours, it is found in the liver, kidney, lung, spleen and skin. Skin, bone and muscle represent the major storage organs. In cases of chronic exposure, arsenic will preferentially accumulate in tissues rich in keratin or sulfhydryl functional groups, such as hair, nails and skin (HBM Commission, 2003). Metabolism of inorganic arsenic begins with a reduction of pentavalent to trivalent arsenic followed by oxidative methylation to monomethylated, dimethylated, and trimethylated products, including MMA and DMA (WHO, 2011). Methylation facilitates the excretion of inorganic arsenic from the body because the end products MMA and DMA are water soluble and readily excreted in urine (WHO, 2001). Absorbed organic arsenic species do not undergo significant metabolism and are predominantly and rapidly eliminated in urine (WHO, 2001).

Biomarkers of arsenic exposure include the levels of arsenic or its metabolites in blood, hair, nails and urine (WHO, 2001). Measurements of speciated metabolites in urine expressed either as inorganic arsenic or as the sum of metabolites (inorganic arsenic + MMA + DMA) are generally accepted as the most reliable indicator of recent arsenic exposure (ATSDR, 2007; WHO, 2001). Measurements of arsenic in urine have been used to identify recent arsenic ingestion or above-average exposures in populations living near industrial point sources of arsenic (ATSDR, 2007).

Acute oral arsenic exposure may cause gastrointestinal effects in humans as well as pain in the extremities and muscles (HC, 2006). These symptoms are often followed by numbness and tingling of the extremities and muscular cramping, and may progress to burning paraesthesias of the extremities, palmoplantar hyperkeratosis, and deterioration in motor and sensory responses (HC, 2006).

Chronic exposure to inorganic arsenic has been associated with decreased lung function, non-cancer skin effects and cardiovascular effects, including increased incidence of high blood pressure and circulatory problems (ATSDR, 2007; EC and HC, 1993). In addition, increased incidences of skin cancer and various cancers of the internal organs have been associated with chronic ingestion of inorganic arsenic-contaminated drinking water (HC, 2006). Much of the evidence on the carcinogenicity of arsenic in humans comes from epidemiological studies conducted in populations consuming high levels of inorganic arsenic through drinking water, including those from Taiwan, Chile and Bangladesh (HC, 2006; 2016). Arsenic and inorganic arsenic compounds are classified as carcinogenic to humans by Health Canada and other international agencies (EPA, 2002; HC, 2006; IARC, 2012). A growing body of evidence suggests that in utero and childhood exposure to high levels of inorganic arsenic may affect fetal and childhood health and development (EFSA CONTAM Panel, 2009; FAO/WHO, 2011; FDA, 2016; NRC, 2013). Although the current amount of information regarding developmental effects in humans is relatively limited and presents some conflicting results, the available data do raise concerns surrounding exposure to inorganic arsenic during critical windows of early development (HC, 2016; Tchounwou et al., 2018). While the majority of assessments of the toxicity of arsenic have focused on the inorganic forms, studies have highlighted the potential for organic arsenic compounds, in particular pentavalent DMA, to be carcinogenic (Cohen et al., 2006; IARC, 2012; Schwerdtle et al., 2003). The International Agency for Research on Cancer (IARC) has classified the methylated arsenic metabolites MMA and DMA as Group 2B, possibly carcinogenic to humans, based on evidence from experimental animals (IARC, 2012). IARC has also evaluated arsenobetaine and other organic arsenic compounds and concluded that they are not classifiable with respect to their carcinogenicity in humans (Group 3) (IARC 2012).

As part of a risk assessment conducted under the mandate of the Canadian Environmental Protection Act, 1999 (CEPA 1999), Health Canada and Environment Canada concluded that arsenic and its inorganic compounds in Canada may be harmful to the environment and may constitute a danger to human life or health (EC and HC, 1993). Inorganic arsenic compounds are listed on Schedule 1, List of Toxic Substances, under CEPA 1999, which allows the federal government to control the importation, manufacture, distribution and use of inorganic arsenic compounds in Canada (Canada, 1999; Canada, 2000). Risk management actions under CEPA 1999 have been developed to control releases of arsenic from thermal electric power generation, base-metal smelting, metal mining, wood preservation and steel manufacturing processes (ECCC, 2017). Arsenic and its compounds are on the List of Ingredients that are Prohibited for Use in Cosmetic Products (HC, 2019). The Food and Drug Regulations prohibit the sale in Canada of drugs for human use containing arsenic or any of its salts or derivatives (Canada, 2012). Further, the leachable arsenic content in a variety of consumer products is regulated under the Canada Consumer Product Safety Act (Canada, 2010a). These regulated consumer products include paints and other surface coatings on cribs, toys and other products for use by children in learning or play situations (Canada, 2010b; Canada, 2011). The sale and use of arsenical pesticides, such as chromated copper arsenate, are regulated in Canada by the Pest Management Regulatory Agency (PMRA) under the Pest Control Products Act (Canada, 2002).

Health Canada, in collaboration with the Federal-Provincial-Territorial Committee on Drinking Water, has developed a guideline for Canadian drinking water quality that establishes a maximum acceptable concentration for arsenic in drinking water (HC, 2006). The guideline was developed based on the incidence of internal (lung, bladder and liver) cancers in humans and the ability of currently available treatment technologies to remove arsenic from drinking water at or below the guideline level (HC, 2006). Arsenic is also included in the list of trace elements analyzed as part of Health Canada's ongoing Total Diet Study surveys (HC, 2020a). The food items analyzed represent those that are most typical of the Canadian diet, and the surveys are used to provide dietary exposure estimates for chemicals that Canadians in different age-sex groups are exposed to through the food supply. The concentration of arsenic in specific foods is managed by Health Canada under the Food and Drug Regulations (Canada, 1978); the existing maximum levels for arsenic in foods are found in the List of Contaminants and Other Adulterating Substances in Foods. Health Canada has updated the maximum level for total arsenic in bottled water and established new maximum levels for inorganic arsenic in rice (HC, 2017; 2020b); maximum levels for other foods and beverages are scheduled for review and update.

Arsenic concentrations in urine have been measured in a number of biomonitoring studies conducted in Canada, including the Maternal–Infant Research on Environmental Chemicals study (Ettinger et al., 2017) and the First Nations Biomonitoring Initiative (AFN, 2013).

Arsenite (III), arsenate (V) and methylated metabolites of arsenic (MMA and DMA) were analyzed individually in the urine of Canadian Health Measures Survey (CHMS) participants aged 3–79 in cycle 2 (2009–2011), cycle 3 (2012– 2013), cycle 4 (2014–2015), cycle 5 (2016–2017) and cycle 6 (2018–2019). Data from these cycles are presented as both µg As/L and µg As/g creatinine. The organoarsenic compounds arsenobetaine and arsenocholine were analyzed together in the urine of CHMS participants aged 3–79 in cycles 2, 3, 4, 5 and 6; arsenocholine was also analyzed alone in cycles 3 and 4. Data from these cycles are presented as both µg As/L and µg As/g creatinine. In addition, total arsenic was measured in the urine of CHMS participants aged 6–79 in cycle 1 and aged 3–79 in cycle 2, and analyzed in hair from CHMS participants aged 20–59 in cycle 5. Finding a measurable amount of arsenic in urine or hair is an indicator of exposure to arsenic and does not necessarily mean that an adverse health effect will occur.

References

• Ackley, K.L., B'Hymer, C., Sutton, K.L., and Caruso, J.A. (1999). Speciation of arsenic in fish tissue using microwave-assisted extraction followed by HPLC-ICP-MS. Journal of Analytical Atomic Spectrometry, 14(5), 845–850.
• AFN (Assembly of First Nations) (2013). First Nations Biomonitoring Initiative: National Results (2011). Assembly of First Nations, Ottawa, ON. Retrieved February 2, 2021.
• ATSDR (Agency for Toxic Substances and Disease Registry) (2007). Toxicological Profile for Arsenic. U.S. Department of Health and Human Services, Atlanta, GA. Retrieved February 22, 2021.
• Batista, B.L., Souza, J.M.O., De Souza, S.S., and Barbosa Jr., F. (2011). Speciation of arsenic in rice and estimation of daily intake of different arsenic species by Brazilians through rice consumption. Journal of Hazardous Materials, 191(1–3), 342–348.
• Canada (1978). Food and Drug Regulations. C.R.C., c. 870. Retrieved February 3, 2021.
• Canada (1999). Canadian Environmental Protection Act, 1999. SC 1999, c. 33. Retrieved February 22, 2021.
• Canada (2000). Order Adding Toxic Substances to Schedule 1 to the Canadian Environmental Protection Act, 1999. Canada Gazette, Part II: Official Regulations, 134(7). Retrieved February 22, 2021.
• Canada (2002). Pest Control Products Act. SC 2002, c. 28. Retrieved February 22, 2021.
• Canada (2010a). Canada Consumer Product Safety Act. SC 2010, c. 21. Retrieved February 22, 2021.
• Canada (2010b). Cribs, Cradles and Bassinets Regulations. SOR/2010-261. Retrieved February 22, 2021.
• Canada (2011). Toys Regulations. SOR/2011-17. Retrieved February 22, 2021.
• Canada (2012). Food and Drug Regulations. C.R.C., c. 870. Retrieved February 22, 2021.
• CCME (Canadian Council of Ministers of the Environment) (1997). Canadian Soil Quality Guidelines for the Protection of Environmental and Human Health – Arsenic (Inorganic). Winnipeg, MB. Retrieved July 12, 2021.
• CFIA (Canadian Food Inspection Agency) (2013). 2010-2011 Arsenic Speciation in Rice and Rice Products, Breakfast and Infant Cereals, Fruit Products, Bottled Water and Seaweed Products. Ottawa, ON. Retrieved February 22, 2021.
• Cohen, S.M., Arnold, L.L., Eldan, M., Lewis, A.S., and Beck, B.D. (2006). Methylated arsenicals: The implications of metabolism and carcinogenicity studies in rodents to human risk assessment. Critical Reviews in Toxicology, 36(2), 99–133.
• Conklin, S.D., and Chen, P.E. (2012). Quantification of four arsenic species in fruit juices by ion-chromatography-inductively coupled plasma-mass spectrometry. Food Additives and Contaminants: Part A, 29(8), 1272–1279.
• EFSA CONTAM Panel (European Food Safety Authority Panel on Contaminants in the Food Chain) (2009). Scientific opinion on arsenic in food. European Food Safety Authority Journal, 7(10), 1351.
• ECCC (Environment and Climate Change Canada) (2017). Toxic substances list: inorganic arsenic compounds. Minister of Environment and Climate Change, Ottawa, ON. Retrieved February 22, 2021.
• EC and HC (Environment Canada and Health Canada) (1993). Priority Substances List Assessment Report: Arsenic and its Compounds. Minister of Supply and Services Canada, Ottawa, ON. Retrieved February 22, 2021.
• EPA (U.S. Environmental Protection Agency) (2002). Integrated Risk Information System (IRIS): Arsenic, inorganic. Office of Research and Development, National Center for Environmental Assessment, Cincinnati, OH. Retrieved February 22, 2021.
• Ettinger, A.S., Arbuckle, T.E., Fisher, M., Liang, C.L., Davis, K., Cirtiu, C.M., Bélanger, P., LeBlanc, A., Fraser, W.D. and MIREC Study Group. (2017). Arsenic levels among pregnant women and newborns in Canada: Results from the Maternal-Infant Research on Environmental Chemicals (MIREC) cohort. Environmental Research, 153, 8-16.
• FAO/WHO (Food and Agriculture Organization of the United Nations/World Health Organization) (2011). Arsenic (addendum). Safety evaluation of certain contaminants in food. Seventy-second meeting of the Joint FAO/WHO Expert Committee on Food Additives. World Health Organization, Geneva. Retrieved February 22, 2021.
• FDA (U.S. Food and Drug Administration) (2016). Arsenic in Rice and Rice Products: Risk Assessment Report. U.S. Department of Health and Human Services, Washington, DC. Retrieved February 22, 2021.
• HBM Commission (Human Biomonitoring Commission of the German Federal Environmental Agency) (2003). Substance Monograph: Arsenic – Reference value in urine. Bundesgesundheitsbl – Gesundheitsforsch – Gesundheitsschutz 2003. 46, 12, 1098–1106 (in German).
• HC (Health Canada) (2006). Guidelines for Canadian Drinking Water Quality: Guideline Technical Document – Arsenic. Minister of Health, Ottawa, ON. Retrieved February 22, 2021.
• HC (Health Canada) (2011). Heavy Duty Wood Preservatives: Creosote, Pentachlorophenol, Chromated Copper Arsenate (CCA) and Ammoniacal Copper Zinc Arsenate (ACZA). Minister of Health, Ottawa, ON. Retrieved February 22, 2021.
• HC (Health Canada) (2016). Scientific assessment in support of a lower tolerance for arsenic in apple juice. Minister of Health, Ottawa, ON. Available upon request.
• HC (Health Canada) (2017). Notice of Modification to the List of Contaminants and Other Adulterating Substances in Foods to Update the Maximum Level for Arsenic in Water in Sealed Containers. Minister of Health, Ottawa, ON. Retrieved February 22, 2021.
• HC (Health Canada) (2019). List of Ingredients that are Prohibited for Use in Cosmetic Products (Hotlist). Minister of Health, Ottawa, ON. Retrieved February 22, 2021.
• HC (Health Canada) (2020a). Concentration of Contaminants and Other Chemicals in Food Composites. Minister of Health, Ottawa, ON. Retrieved February 22, 2021.
• HC (Health Canada) (2020b). Notice of Modification to Add Maximum Levels for Inorganic Arsenic in Polished (White) and Husked (Brown) Rice to Part 2 of the List of Contaminants and Other Adulterating Substances in Foods. Minister of Health, Ottawa, ON. Retrieved January 25, 2021.
• Huang, J.H., Fecher, P., Ilgen, G., Hu, K.N., and Yang, J. (2012). Speciation of arsenite and arsenate in rice grain – Verification of nitric acid based extraction method and mass sample survey. Food Chemistry, 130(2), 453–459.
• IARC (International Agency for Research on Cancer) (2012). IARC Monographs on the Evaluation of Carcinogenic Risks to Humans – Volume 100C: Arsenic, Metals, Fibres, and Dusts. World Health Organization, Lyon. Retrieved February 22, 2021.
• Leufroy, A., Noel, L., Dufailly, V., Beauchemin, D., and Guerin, T. (2011). Determination of seven arsenic species in seafood by ion exchange chromatography coupled to inductively coupled plasma-mass spectrometry following microwave assisted extraction: Method validation and occurrence data. Talanta, 83(3), 770–779.
• NRC (National Research Council) (2013). Critical Aspects of EPA's IRIS Assessment of Inorganic Arsenic: Interim Report. Washington, DC. Retrieved February 22, 2021.
• Rasmussen, P.E., Subramanian, K.S., and Jessiman, B.J. (2001). A multi-element profile of house dust in relation to exterior dust and soils in the city of Ottawa, Canada. Science of the Total Environment, 267(1), 125–140.
• Ruttens, A., Blanpain, A.C., De Temmerman, L., and Waegeneers, N. (2012). Arsenic speciation in food in Belgium: Part 1: Fish, molluscs and crustaceans. Journal of Geochemical Exploration, 121, 55–61.
• Schwerdtle, T., Walter, I., Mackwin, I., and Hartwig, A. (2003). Induction of oxidative DNA damage by arsenite and its trivalent and pentavalent methylated metabolites in cultured human cells and isolated DNA. Carcinogenesis, 24(5), 967–974.
• Tchounwou, P.B., Yedjou, C.G., Udensi, U.K., Pacurari, M., Stevens, J.J., Patlolla, A.K., Noubissi, F., Kumar, S. (2018). State of the science review of the health effects of inorganic arsenic: Perspectives for future research. Environmental Toxicology, 34(2), 203-209
• WHO (World Health Organization) (2001). Environmental Health Criteria 224: Arsenic and arsenic compounds. WHO, Geneva. Retrieved February 22, 2021.
• WHO (World Health Organization) (2011). Guidelines for drinking-water quality, fourth edition. WHO, Geneva. Retrieved February 22, 2021.

8.3 Boron

Boron (CASRN 7440-42-8) is a naturally occurring element. It is a metalloid exhibiting properties intermediate between those of typical metals and nonmetals. Elemental boron exists in a crystalline or amorphous form; however, it is never found in nature in the free elemental form (Ince et al., 2017; WHO, 2009; ATSDR, 2010). Boron is always found in combination with oxygen as borate compounds, including boric acid, sodium tetraborate (or Borax) and boron oxide (ATSDR, 2010).

Boron is widely distributed in nature and can be released by both natural and anthropogenic processes. Volcanic emissions, sea salt aerosol, soil dust, plant aerosols and weathering of soil and rocks containing borates are important sources of natural borates released into the environment (Canada, 2016; HC, 2016; 2020). Anthropogenic sources include the manufacture, import and use of boric acid, its salts and its precursors in manufactured products and applications such as fibreglass insulation, oil and gas extraction, fertilizers, cellulose insulation, gypsum boards, engineered wood products, pulp and paper manufacturing, rubber manufacturing, chemical manufacturing, metallurgical applications and cleaning products. Other anthropogenic sources include the incidental production and subsequent release of boric acid as a result of activities such as coal-fired power generation, metal mining, smelting and refining, coal mining, oil sands extraction and processing, oil and gas extraction, wastewater treatment and waste disposal (ECCC and HC, 2016).

Exposure to boron occurs primarily through the ingestion of food (mainly fruit and vegetables) and drinking water (ATSDR, 2010; Canada, 2016). The range of boron concentrations in these media varies widely across the world (WHO, 2009; Canada, 2016). Boron is generally not present at significant levels in air because of the low volatility of borate compounds (WHO, 2009). Exposure to borates can also occur through products available to consumers such as cosmetics, arts and craft materials, toys, natural health products, cleaning products and swimming pool products, as well as through the use of household pest control products (Canada, 2016; ECCC and HC, 2016; HC, 2016).

Inorganic borates are readily absorbed across mucous membranes; gastrointestinal absorption has been estimated at approximately 81% to 92% (ATSDR, 2010; Devirian and Volpe, 2003; Dourson et al., 1998). Significant absorption can also occur through inhalation (Ince et al., 2017). Dermal absorption is generally low in healthy skin (~0.5% to 10%), but can be significantly increased in damaged skin (ECCC and HC, 2016; Ince et al., 2017). Boron is mostly present in the body as boric acid; borates are rapidly converted to boric acid in the mucosal layer before rapid absorption and distribution (Devirian and Volpe, 2003). Animal studies show that absorbed boric acid is equally distributed to liver, kidneys, genital tissue, brain, adrenals, muscles and blood (Ince et al., 2017). Boron can also cross the placental barrier; some animal toxicology studies have reported accumulation in bone over long-term oral exposure (Ince et al., 2017). Boric acid is not further metabolized in the bodies of humans or animals because substantial energy is required to break the oxygen and boron bond (Ince et al., 2017). Consequently, orally absorbed boric acid is rapidly eliminated unchanged, mainly in urine, with a half-life of less than 24 hours (Ince et al., 2017). A small amount is found in feces (2%) and a smaller amount in bile, sweat and breath (Devirian and Volpe, 2003). Measurement of inorganic borates in urine reflects boron intake, and is an indicator of human exposure (Devirian and Volpe, 2003). Boron in blood can also be used to estimate human exposure (ATSDR, 2010; ECCC and HC, 2016).

Although boron plays important roles in human health — being involved in functions such as bone growth, regulation of sex hormones and anti-inflammatory and anti-cancer effects — it is not considered an essential trace element in humans at this time (Devirian and Volpe, 2003; IOM, 2001; Pizzorno, 2015). The acute oral toxicity of boron is generally low (Hubbard, 1998). Acute toxicity is more likely in children, the elderly and people with kidney problems. Symptoms may include vomiting, nausea, digestive disorders, skin flushing, ataxia, headache, seizure, depression, vascular collapse and death (Devirian and Volpe, 2003; ECCC and HC, 2016; HC, 2020; Ince et al., 2017). Acute inhalation toxicity marked by irritation of the respiratory tract and eyes has been reported in boron production workers following occupational exposure to borate dusts (ATSDR, 2010).

Chronic exposure to boron has been associated with digestive problems (nausea, vomiting and loss of appetite) as well as nervous system irritation and convulsion. Subchronic and chronic experimental animal studies suggest that high-dose exposure to boron compounds leads to reproductive and developmental toxicity, particularly affecting the male reproductive system (Devirian and Volpe, 2003; ECCC and HC, 2016; HC, 2020; Hubbard, 1998; Ince et al., 2017). Evidence for the effects of boron on human reproduction and development is less clear (ECCC and HC, 2016; HC, 2020; Ince et al., 2017; Scialli et al., 2010). There is no conclusive evidence for mutagenic or genotoxic effects of boron (Hubbard, 1998; Ince et al., 2017); consequently, boron is not classified as a carcinogen by the International Agency for Research on Cancer or other agencies (ATSDR, 2010).

The Government of Canada has conducted a science-based screening assessment under the Chemicals Management Plan to determine whether boric acid, its salts and its precursors present or may present a risk to the environment or human health as per the criteria set out in section 64 of the Canadian Environmental Protection Act, 1999 (CEPA 1999) (Canada, 1999; ECCC and HC, 2016). The draft assessment proposed to conclude that boric acid, its salts and its precursors are toxic under CEPA 1999 because they are considered harmful to the environment and human health (ECCC and HC, 2016).

The sale and use of pesticides are regulated in Canada by the Pest Management Regulatory Agency (PMRA) under the Pest Control Products Act (Canada, 2002). Based on a re-evaluation by the PMRA in 2016, most pesticides containing boric acid and its salts continue to be approved, as they pose no unacceptable risk for humans or the environment when they are used according to revised label directions (HC, 2016). However, a number of pesticide products that contain boric acid for use in and around the home that are in powder form or in other formulations carrying a potential risk for overexposure will be phased out of the marketplace (HC, 2016). Boric acid and its salts are on the List of Ingredients that are Restricted for Use in Cosmetic Products (HC, 2019). Canada's Food and Drug Regulations specify that a cautionary statement must appear on the label of drug products containing boric acid or sodium borate to prevent administration to children under the age of 3 (Canada, 1985). Toy Regulations under the Canada Consumer Product Safety Act prohibit the presence of boron in children's toys (Canada, 2016).

Health Canada, in collaboration with the Federal-Provincial-Territorial Committee on Drinking Water, has developed a Canadian drinking water quality guideline that proposed a maximum acceptable concentration for boron in drinking water (HC, 2020). The guideline was proposed based on the achievability of water treatment to reduce boron (HC, 2020).

Boron was analyzed in the urine of Canadian Health Measures Survey (CHMS) cycle 5 (2016–2017) and cycle 6 (2018–2019) participants aged 3–79. Data from this cycle are presented in urine as both µg/L and µg/g creatinine. Finding a measurable amount of boron in urine is an indicator of exposure to boron and does not necessarily mean that an adverse health effect will occur.

References

• ATSDR (Agency for Toxic Substances and Disease Registry) (2010). Toxicological Profile for Boron. U.S Department of Health and Human Services, Atlanta, GA. Retrieved February 22, 2021.
• Canada (1985). Food and Drugs Act. RSC 1985, c. F-27. Retrieved February 22, 2021.
• Canada (1999). Canadian Environmental Protection Act, 1999. SC 1999, c. 33. Retrieved February 22, 2021.
• Canada (2002). Pest Control Products Act. SC 2002, c. 28. Retrieved February 22, 2021.
• Canada (2016). Boric Acid, its salts and precursors. Retrieved February 22, 2021.
• Devirian, T.A., and Volpe, S.L. (2003). The physiological effects of dietary boron. Critical Reviews in Food Science and Nutrition, 43 (2), 219–231.
• Dourson, M., Maier, A., Meek, B., Renwick, A., Ohanian, E., and Poirier, K. (1998). Boron tolerable intake: re-evaluation of toxicokinetics for data-derived uncertainty factors. Biological trace element research, 66(1-3), 453–463.
• ECCC and HC (Environment and Climate Change Canada and Health Canada) (2016). Draft Screening Assessment: Boric Acid, its Salts and its Precursors. Minister of Environment and Climate Change, Ottawa, ON. Retrieved February 22, 2021.
• HC (Health Canada) (2016). Re-evaluation Decision RVD2016-01, Boric Acid and its Salts (Boron). Minister of Health, Ottawa, ON. Retrieved February 22, 2021.
• HC (Health Canada) (2019). List of Ingredients that are Restricted for Use in Cosmetic Products (Hotlist). Minister of Health, Ottawa, ON. Retrieved February 22, 2021.
• HC (Health Canada) (2020). Boron in Drinking Water – Guideline Technical Document for Public Consultation. Minister of Health, Ottawa, ON. Retrieved October 21, 2020.
• Hubbard, S.A. (1998). Comparative toxicology of borates. Biological Trace Element Research, 66(1–3), 343–357.
• Ince, S., Filazi, A., and Yurdakok-Dikmen, B. (2017). Boron. Reproductive and Developmental Toxicology (Second Edition). Elsevier. Pages 521–535.
• IOM (Institute of Medicine) (2001). Dietary reference intakes for vitamin A, vitamin K, arsenic, boron, chromium, copper, iodine, iron, manganese, molybdenum, nickel, silicon, vanadium, and zinc. Washington, DC: National Academies Press.
• Pizzorno, L. (2015). Nothing boring about boron. Integrative Medicine: A Clinician's Journal, 14(4), 35.
• Scialli, A.R., Bonde, J.P., Brüske-Hohlfeld, I., Culver, B.D., Li, Y., and Sullivan, F.M. (2010). An overview of male reproductive studies of boron with an emphasis on studies of highly exposed Chinese workers. Reproductive Toxicology, 29(1), 10–24.
• WHO (World Health Organization) (2009). Boron in Drinking-water: Background document for development of WHO Guidelines for Drinking-water Quality. World Health Organization, Geneva. Retrieved February 22, 2021.

8.4 Cadmium

Cadmium (CASRN 7440-43-9) is a naturally occurring, soft, silvery white, blue-tinged metal. Common forms include soluble species (e.g., cadmium chloride, cadmium sulfate) and insoluble species (e.g., cadmium metal and its oxides) that may also be found as particulate matter in the atmosphere (ATSDR, 2012; CCME, 1999).

Cadmium is released into the environment as a result of natural processes, including forest fires, volcanic emissions and weathering of soil and bedrock (Morrow, 2000). The main anthropogenic sources of atmospheric cadmium are industrial base-metal smelting and refining processes and combustion processes (such as coal-fired electrical plants and waste incineration) where cadmium is released as a by-product (CCME, 1999).

Cadmium is primarily used in the manufacture of nickel-cadmium batteries. It is also used in industrial coatings and electroplating, in pigments and as a stabilizer in polyvinyl chloride plastics (ATSDR, 2012). Cadmium is present in metal alloy sheets, wires, rods, solders and shields for various industrial applications (EC and HC, 1994). It is also sometimes used in costume jewellery and as a pigment in ceramic glazes. Cadmium may also be present in fertilizers. It is frequently found as an impurity in galvanized pipes and well components, brass fittings and cement-mortar linings, and is a constituent of solders used in plumbing. Cadmium in drinking water results primarily from the deterioration of galvanized steel pipes and well components and, to a lesser extent, leaching from brass materials and cement-mortar linings (HC, 2020b; WHO, 2011).

In smokers, inhalation of cigarette smoke is a major source of cadmium exposure (EC and HC, 1994; IARC, 2012). For non-smoking adults and children, the largest source of cadmium exposure is food (EC and HC, 1994; IARC, 2012). Ambient air is usually a minor source of exposure, with intakes estimated to be 2 to 3 orders of magnitude lower than for food, although cadmium compounds are more readily absorbed following inhalation than through ingestion (Friberg, 1985). Other potential sources of exposure include ingestion of drinking water, soil or dust (ATSDR, 2012; HC, 2020b; Rasmussen et al., 2013).

Absorption of dietary cadmium into the bloodstream depends on one's nutritional status and the levels of other components of the diet, such as iron, calcium and protein. The majority of dietary cadmium is not absorbed; average gastrointestinal absorption is estimated at 5% in adult men and 10% or higher in adult women (CDC, 2009). About 25% to 60% of inhaled cadmium is absorbed through the lungs (ATSDR, 2012). Absorbed cadmium accumulates mainly in the kidneys and liver, with approximately one-third to one-half of the total body burden accumulating in the kidneys (CDC, 2009). The biological half-life of cadmium in the kidneys has been estimated to be approximately 10 to 12 years (Amzal et al., 2009; Lauwerys et al., 1994). Only a small proportion of absorbed cadmium is eliminated, mainly in urine and feces, with small amounts also eliminated through hair, nails and sweat.

Cadmium can be measured in blood, urine, feces, liver, kidney, hair and other tissues. Cadmium concentrations in urine best reflect cumulative exposure and the concentration of cadmium in the kidneys, although slight fluctuations occur with recent exposures (Adams and Newcomb, 2014). Concentrations in blood reflect more recent exposures (Adams and Newcomb, 2014). Blood cadmium concentrations are about twice as high in smokers compared with non-smokers; concentrations can also be elevated following occupational exposures (ATSDR, 2012).

Oral exposure to high doses of cadmium may cause severe gastrointestinal irritation and kidney effects (ATSDR, 2012). Chronic exposure via inhalation has been associated with effects in the lungs (including emphysema) and kidneys (ATSDR, 2012). The kidney is considered the critical organ that exhibits the first adverse effects after either oral or inhalation exposure, based on observations in both human epidemiology and animal toxicity studies (EFSA, 2009; FAO/WHO, 2011; ATSDR, 2012).

Inhaled cadmium and its compounds have been classified as probably carcinogenic to humans by Environment Canada and Health Canada (EC and HC, 1994). More recently, the International Agency for Research on Cancer has classified cadmium and its compounds as carcinogenic to humans (Group 1) based on various data, including associations between occupational inhalation exposure and lung cancer (IARC, 2012). There is insufficient evidence to determine whether or not cadmium is carcinogenic in humans following oral exposure (ATSDR, 2012).

Health Canada and Environment Canada concluded that inorganic cadmium compounds may be harmful to the environment and may constitute a danger to human life or health in Canada (EC and HC, 1994). Inorganic cadmium compounds are listed on Schedule 1, List of Toxic Substances, under the Canadian Environmental Protection Act, 1999 (CEPA 1999). The act allows the federal government to control the importation, manufacture, distribution and use of inorganic cadmium compounds in Canada (Canada, 1999; Canada, 2000). Risk management actions under CEPA 1999 have been developed to control releases of cadmium from thermal electric power generation, base-metal smelting and steel manufacturing processes (EC, 2013).

Cadmium is included in the list of trace elements analyzed as part of Health Canada's ongoing Total Diet Study surveys (HC, 2020a). The food items analyzed represent those that are most typical of the Canadian diet, and these surveys are used to provide dietary exposure estimates for chemicals to which Canadians in different age-sex groups are exposed through the food supply. On the basis of data collected, Health Canada has concluded that dietary exposure to cadmium does not represent a health concern for the general Canadian population (HC, 2018). In Canada, the leachable cadmium content in a variety of consumer products is regulated under the Canada Consumer Product Safety Act (Canada, 2010a). Consumer products regulated for leachable cadmium content include glazed ceramics and glassware, as well as paints and other surface coatings on cribs, toys, and other products for use by a child in learning or play situations (Canada, 1998; 2010b; 2011; HC, 2009). In addition, because children's jewellery items containing high levels of cadmium have been found in the Canadian marketplace, a guideline limit for total cadmium in children's jewellery was finalized and published in 2018 as part of the Children's Jewellery Regulations under the Canada Consumer Product Safety Act (Canada, 2018). Cadmium and its compounds are on the List of Ingredients that are Prohibited for Use in Cosmetic Products (HC, 2019). On the basis of health considerations, Health Canada, in collaboration with the Federal-Provincial-Territorial Committee on Drinking Water, has developed a guideline for Canadian drinking water quality that establishes the maximum acceptable concentration for cadmium in drinking water (HC, 2020b).

Cadmium concentrations in blood and urine have been measured in a number of biomonitoring studies conducted in Canada, including the Maternal–Infant Research on Environmental Chemicals study (Arbuckle et al., 2016) and the First Nations Biomonitoring Initiative (AFN, 2013).

Cadmium was analyzed in the whole blood of Canadian Health Measures Survey (CHMS) participants aged 6–79 in cycle 1 (2007–2009), and aged 3–79 in cycle 2 (2009–2011), cycle 3 (2012–2013), cycle 4 (2014–2015), cycle 5 (2016–2017) and cycle 6 (2018–2019). Data from these cycles are presented in blood as µg/L. Cadmium was analyzed in the urine of CHMS participants aged 6–79 in cycle 1, and aged 3–79 in cycles 2, 5 and 6. Data from these cycles are presented in urine as both µg/L and µg/g creatinine. Cadmium was also analyzed in hair from CHMS participants aged 20–59 in cycle 5. Finding a measurable amount of cadmium in blood, urine or hair is an indicator of exposure to cadmium, and does not necessarily mean that an adverse health effect will occur.

References

• Adams, S.V., and Newcomb, P.A. (2014). Cadmium blood and urine concentrations as measures of exposure: NHANES 1999–2010. Journal of Exposure Science and Environmental Epidemiology, 24(2), 163–170.
• AFN (Assembly of First Nations) (2013). First Nations Biomonitoring Initiative: National Results (2011). Assembly of First Nations, Ottawa, ON. Retrieved February 2, 2021.
• Amzal, B., Julin, B., Vahter, M., Wolk, A., Johanson, G., and Akesson, A. (2009). Population toxicokinetic modeling of cadmium for health risk assessment. Environmental Health Perspectives, 117(8), 1293–1301.
• Arbuckle, T.E., Liang, C.L., Morisset, A.S., Fisher, M., Weiler, H., Cirtiu, C.M., Legrand, M., Davis, K., Ettinger, A.S., Fraser, W.D., et al. (2016). Maternal and fetal exposure to cadmium, lead, manganese and mercury: The MIREC study. Chemosphere, 163, 270–282.
• ATSDR (Agency for Toxic Substances and Disease Registry) (2012). Toxicological Profile for Cadmium. U.S. Department of Health and Human Services, Atlanta, GA. Retrieved February 23, 2021.
• Canada (1998). Glazed Ceramics and Glassware Regulations. SOR/98-176. Retrieved February 23, 2021.
• Canada (1999). Canadian Environmental Protection Act, 1999. SC 1999, c. 33. Retrieved February 23, 2021.
• Canada (2000). Order Adding Toxic Substances to Schedule 1 to the Canadian Environmental Protection Act, 1999. Canada Gazette, Part II: Official Regulations, 134(7). Retrieved February 23, 2021.
• Canada (2010a). Canada Consumer Product Safety Act. SC 2010, c. 21. Retrieved February 23, 2021.
• Canada (2010b). Cribs, Cradles and Bassinets Regulations. SOR/2010-261. Retrieved February 23, 2021.
• Canada (2011). Toys Regulations. SOR/2011-17. Retrieved February 23, 2021.
• Canada (2018). Children's Jewellery Regulations. SOR/2018-82. Retrieved February 23, 2021.
• CCME (Canadian Council of Ministers of the Environment) (1999). Canadian Soil Quality Guidelines for the Protection of Environmental and Human Health – Cadmium. Winnipeg, MB. Retrieved July 12, 2021.
• CDC (Centers for Disease Control and Prevention) (2009). Fourth National Report on Human Exposure to Environmental Chemicals. Department of Health and Human Services, Atlanta, GA. Retrieved February 23, 2021.
• EFSA (European Food Safety Authority) (2009). Technical report of EFSA prepared by the assessment methodology unit on meta-analysis of dose-effect relationship of cadmium for benchmark dose evaluation. European Food Safety Authority Journal, 254, 1–62.
• EC (Environment Canada) (2013). Toxic substances list: inorganic cadmium compounds. Minister of the Environment, Ottawa, ON. Retrieved February 23, 2021.
• EC and HC (Environment Canada and Health Canada) (1994). Priority Substances List Assessment Report: Cadmium and its compounds. Minister of Supply and Services Canada, Ottawa, ON. Retrieved February 23, 2021.
• FAO/WHO (Food and Agriculture Organization of the United Nations/World Health Organization) (2011). Cadmium (addendum). Safety evaluation of certain food additives and contaminants. Seventy-third meeting of the Joint FAO/WHO Expert Committee on Food Additives, World Health Organization, Geneva. Retrieved February 23, 2021.
• Friberg, L. (1985). Cadmium and health: A toxicological and epidemiological appraisal. CRC Press, Boca Raton, FL.
• HC (Health Canada) (2009). Notice regarding Canada's legislated safety requirements related to heavy metal content in surface coating materials applied to children's toys. Minister of Health, Ottawa, ON.
• HC (Health Canada) (2018). Health risk assessment of dietary exposure to cadmium. Minister of Health, Ottawa, ON. Available upon request.
• HC (Health Canada) (2019). List of Ingredients that are Prohibited for Use in Cosmetic Products (Hotlist). Minister of Health, Ottawa, ON. Retrieved February 23, 2021.
• HC (Health Canada) (2020a). Concentration of Contaminants and Other Chemicals in Food Composites. Minister of Health, Ottawa, ON. Retrieved February 23, 2021.
• HC (Health Canada) (2020b). Guidelines for Canadian Drinking Water Quality: Guideline Technical Document – Cadmium. Minister of Health, Ottawa, ON. Retrieved March 23, 2021.
• IARC (International Agency for Research on Cancer) (2012). IARC Monographs on the Evaluation of Carcinogenic Risks to Humans – Volume 100C: Arsenic, Metals, Fibres, and Dusts. World Health Organization, Lyon. Retrieved February 23, 2021.
• Lauwerys, R.R., Bernard, A.M., Roels, H.A., and Buchet, J.P. (1994). Cadmium: Exposure markers as predictors of nephrotoxic effects. Clinical Chemistry, 40(7), 1391–1394.
• Morrow, H. (2000). Cadmium and cadmium alloys. Kirk-Othmer Encyclopedia of Chemical Technology. John Wiley and Sons, Inc., Mississauga, ON.
• Rasmussen, P.E., Levesque, C., Chénier, M., Gardner, H.D., Jones-Otazo, H., and Petrovic, S. (2013). Canadian House Dust Study: Population-based concentrations, loads and loading rates of arsenic, cadmium, chromium, copper, nickel, lead, and zinc inside urban homes. Science of the Total Environment, 443, 520–529.
• WHO (World Health Organization) (2011). Cadmium in Drinking-water: Background document for development of WHO Guidelines for Drinking-water Quality. WHO, Geneva. Retrieved February 23, 2021.

8.5 Chromium

Chromium (CASRN 7440-47-3) is a naturally occurring element. It is a transition metal that exhibits different properties depending on its oxidation state. Chromium can exist in 9 different oxidation states, with the trivalent (chromium [III]) and the hexavalent (chromium [VI]) forms found most commonly in the environment (EC an HC, 1994; HC, 2018). In nature, chromium is not found in its elemental form, but rather in complexes with oxygen, iron or lead (HC, 2018).

Chromium is released into the environment by both natural and anthropogenic processes. Natural processes include weathering and erosion of soil and rocks as well as volcanic emissions (WHO, 2003; HC, 2018). More than 70% of chromium released into air, soil and water comes from anthropogenic sources, such as smelting and refining of nonferrous base metals, the production and combustion of fossil fuels, industrial manufacturing, and processing of chromium-based products (ATSDR, 2012; HC, 2018; ECCC, 2017). Chromium (VI) rarely occurs naturally. It is produced mainly during the reduction of chromite ore in the industrial production of chromium metal. This oxidation state represents one-third of the total anthropogenic chromium released into the atmosphere (ATSDR, 2012; IARC, 2012).

Chromium is primarily used in electrical applications, wood preservation, the automobile industry and the metallurgical industry, where it is used to produce stainless steel and high-chromium cast iron alloys (ATSDR, 2012; HC, 2018). It is also used in many other processes, such as the production of paint, textile dyes and mordants, catalysts, pulp and paper, as well as in leather tanning, electroplating, and clinical medicine (HC, 2018; WHO, 2003).

While exposure to chromium (III) occurs mainly through food, exposure to chromium (VI) occurs through drinking water and ambient air (HC, 2018; IARC, 2012). However, the majority of drinking water samples analyzed for total chromium across Canada were found to be below the detection limit (HC, 2018). Inhalation of chromium occurs mainly from cigarette smoke or from living near a contaminated area or an emission source, such as an industrial facility. Dermal exposure occurs through the use of consumer products containing chromium, including cleaning materials, textiles and leather (ATSDR, 2012).

Chromium (III) is an essential nutrient that plays a role in human metabolism, while chromium (VI) is the oxidation state that poses the greatest health risk (ATSDR, 2012; Dayan and Paine, 2001; IOM, 2001). As such, the summary of toxicokinetics and health effects will focus on chromium (VI).

Chromium (VI) can be absorbed after oral or inhalation exposure. Absorption from the gastrointestinal tract is low (~7%), and chromium (VI) is partially reduced to chromium (III) at the intragastric level, which lowers its absorption (HC, 2018; IARC, 2012; WHO, 2003). Chromium (VI) is readily absorbed via inhalation, but the fraction absorbed depends on several factors, such as the properties of the inhaled particles and the degree of reduction of chromium (VI) to chromium (III). Significant dermal absorption of chromium (VI) can occur, especially in damaged skin (ATSDR, 2012). After absorption into the bloodstream, chromium (VI) is taken up into red blood cells, where it is reduced to chromium (III), bound to hemoglobin and other intracellular proteins, and slowly lost from the cell (ATSDR, 2012; Dayan and Paine, 2001; IARC, 2012). Generally speaking, chromium (VI) is unstable in the body and is reduced to chromium (III), which can lead to the formation of reactive intermediates, chromium adducts with proteins and DNA, and secondary free radicals (ATSDR, 2012). Chromium is distributed to nearly all tissues, including blood, liver, lung, spleen and kidney, and has a half-life in blood of about 30 days (EPA, 1998; HC, 2018; WHO, 2003). Chromium can be transferred to infants via the placenta and breast milk (ATSDR, 2012). Elimination of chromium (VI) absorbed by inhalation occurs mainly in urine as the trivalent form (HC, 2018; WHO, 2003), whereas after oral exposure, excretion occurs mainly through feces (IARC, 2012).

Measured levels of chromium in urine, whole blood, plasma, red blood cells and lymphocytes can be used as biomarkers of exposure (ATSDR, 2012; Devoy et al., 2016). As chromium (III) is not able to cross the red blood cell membrane, chromium measured in red blood cells is a specific marker of chromium (VI) exposure, whereas the level of total chromium in urine may reflect either chromium (III) or chromium (VI) exposure (Devoy et al., 2016).

The toxicity of chromium depends upon its form and the route of exposure (HC, 2018). Acute toxicity resulting from ingestion of chromium (VI) can occur at high doses, leading to gastrointestinal, kidney, liver and respiratory disorders, hemorrhagic diathesis, convulsions and, at very high concentrations, death from cardiovascular shock (HC, 2018; WHO, 2003). There is a lack of clear evidence for chronic non-cancer toxicity from oral ingestion of chromium. However, chronic inhalation exposure of workers to chromium (VI) has been associated with respiratory tract effects, including nose bleeds, irritations or atrophy of the lining of the nose, bronchitis and pneumonia (ATSDR, 2012). Dermal disorders, such as chronic skin ulcers or acute irritative dermatitis, have been reported in workers dermally exposed to chromium-containing material (Dayan and Paine, 2001).

There is limited information on the reproductive toxicity of chromium (VI) in humans, but some studies suggest that occupational exposure in males may lead to abnormal sperm count, morphology and motility (ATSDR, 2012). Occupational exposure studies have also demonstrated genotoxic effects of chromium (VI) and its compounds (ATSDR, 2012). Several epidemiological studies in workers employed in chromate production, chromate pigment production or chromium electroplating have reported that inhalation of chromium (VI) is associated with lung cancer and possibly cancer of the nose and nasal sinuses (HC, 2018; IARC, 2012; WHO, 2003). The International Agency for Research on Cancer has classified chromium (VI) compounds as carcinogenic to humans (Group 1) based on sufficient evidence for carcinogenicity (lung cancer) in both humans and experimental animals (IARC, 2012).

Health Canada and Environment Canada concluded that chromium (VI) compounds may be harmful to the environment and may constitute a danger to human life or health (EC and HC, 1994). Chromium (VI) and its compounds have been added to the List of Toxic Substances under Schedule 1 of the Canadian Environmental Protection Act, 1999 (CEPA 1999) (Canada, 1999). The act allows the federal government to control the importation, manufacture, distribution and use of chromium (VI) compounds in Canada. Risk management actions, including regulations and emission guidelines, have been developed under CEPA 1999 to control the release of chromium (VI) from thermal electricity generation, wood preservation applications, electroplating, anodizing and reverse etching (ECCC, 2017). Chromium, chromic acid and its salts are on the List of Ingredients that are Prohibited for Use in Cosmetic Products (HC, 2019).

On the basis of health considerations, Health Canada, in collaboration with the Federal-Provincial-Territorial Committee on Drinking Water, has developed a guideline for Canadian drinking water quality that establishes the maximum acceptable concentration for total chromium in drinking water (HC, 2018). The guideline also takes into account the ability of currently available treatment technologies to remove chromium from drinking water at or below the guideline level.

Chromium was measured in the red blood cells of Canadian Health Measures Survey (CHMS) participants aged 3–79 in cycle 5 (2016–2017) and cycle 6 (2018–2019). Data are presented as µg/L red blood cells. Chromium (VI) is the only form of inorganic chromium that substantially penetrates red blood cells. Thus, finding a measurable amount of chromium in red blood cells is an indicator of recent exposure. In addition, total chromium was analyzed in hair from CHMS participants aged 20–59 in cycle 5. The presence of chromium in red blood cells or hair does not necessarily mean that an adverse health effect will occur.

References

• ATSDR (Agency for Toxic Substances and Disease Registry) (2012). Toxicological Profile for Chromium. U.S. Department of Health and Human Services, Atlanta, GA. Retrieved February 23, 2021.
• Canada (1999). Canadian Environmental Protection Act, 1999. SC 1999, c33 C.F.R. Retrieved February 23, 2021.
• Dayan, A., and Paine, A. (2001). Mechanisms of chromium toxicity, carcinogenicity and allergenicity: review of the literature from 1985 to 2000. Human and experimental toxicology, 20(9), 439–451.
• Devoy, J., Géhin, A., Müller, S., Melczer, M., Remy, A., Antoine, G., and Sponne, I. (2016). Evaluation of chromium in red blood cells as an indicator of exposure to hexavalent chromium: An in vitro study. Toxicology letters, 255, 63–70.
• ECCC (Environment and Climate Change Canada) (2017). Hexavalent chromium compounds. Minister of Environment and Climate Change, Ottawa, ON. Retrieved February 23, 2021.
• EC and HC (Environment Canada and Health Canada) (1994). Priority Substances List Assessment Report: Chromium and its Compounds. Minister of Supply and Services Canada, Ottawa, ON. Retrieved February 23, 2021.
• EPA (U.S. Environmental Protection Agency) (1998). Toxicological Review of Hexavalent Chromium. Washington, DC. Retrieved February 23, 2021.
• HC (Health Canada) (2018). Guidelines for Canadian Drinking Water Quality: Guideline Technical Document – Chromium. Minister of Health, Ottawa, ON. Retrieved March 23, 2021.
• HC (Health Canada) (2019). List of Ingredients that are Prohibited for Use in Cosmetic Products (Hotlist). Minister of Health, Ottawa, ON. Retrieved February 23, 2021.
• IARC (International Agency for Research on Cancer) (2012). IARC Monographs on the Evaluation of Carcinogenic Risks to Humans — Volume 100C: Arsenic, Metals, Fibres and Dusts. World Health Organization, Lyon. Retrieved February 23, 2021.
• IOM (Institute of Medicine) (2001). Dietary reference intakes for vitamin A, vitamin K, arsenic, boron, chromium, copper, iodine, iron, manganese, molybdenum, nickel, silicon, vanadium, and zinc. The National Academies Press, Washington, DC.
• WHO (World Health Organization) (2003). Chromium in Drinking-water: Background document for development of WHO Guidelines for Drinking-water Quality. WHO, Geneva. Retrieved July 13, 2021.

8.6 Mercury

Mercury (CASRN 7439-97-6) is a naturally occurring, soft, silvery white metal that is liquid at room temperature. Mercury exists in elemental, inorganic and organic forms. Elemental and certain organic forms of mercury have sufficiently high vapour pressures to be present as vapour in ambient air (ATSDR, 1999; 2013). The most common organic mercury compounds in nature are methylmercury (monomethylmercury) and dimethylmercury. Mercury can be converted among its elemental, inorganic and organic forms by a variety of processes, including biological transformation (ECCC, 2017).

Mercury is found throughout the environment, including in remote Arctic regions, because of its persistence, mobility and tendency to accumulate in colder climates. Natural sources of inorganic mercury include volcanic activity and natural erosion of mercury-containing deposits (EC and HC, 2010). Anthropogenic sources of inorganic mercury include artisanal and small-scale gold mining; coal burning; the mining, smelting and production of iron and non-ferrous metals; cement production; industrial point sources such as power plants or factories; contaminated sites such as old mines, landfills, and waste disposal locations; and sewage sludge and wastewater (UNEP, 2013). Inorganic mercury may also be released to the environment following disposal of products containing mercury. Metabolism of inorganic mercury by microorganisms in the environment creates organic mercury (e.g., methylmercury), which often bioaccumulates in terrestrial and aquatic food chains (ATSDR, 1999; 2013).

Mercury has unique properties that have made it useful in certain products, such as wiring devices, switches and scientific measuring devices, including vacuum gauges and thermometers (ATSDR, 1999; 2013). Today, the manufacture and import of most mercury-containing products is prohibited in Canada. Exemptions include certain essential products, such as certain medical and research applications, dental amalgams, and fluorescent and other types of lamps (Canada, 2014). Mercury is also used as an industrial catalyst and in laboratory reagents, disinfectants, embalming solutions and some pharmaceuticals. A significant use of inorganic mercury is in dental amalgam, which is composed of approximately 50% mercury (IMERC, 2010; SCENIHR, 2015). Based on data collected as part of the Canadian Health Measures Survey (CHMS) cycle 1 (2007–2009), it was estimated that approximately 64% of the Canadian population age 6 and over had 1 or more amalgam-restored tooth surfaces (Richardson, 2014). A review of these same data concluded that urinary mercury concentrations in the general Canadian population were significantly lower than the values considered to pose any health risks (Nicolae et al., 2013).

Mercury exposure in Canada's general population is primarily through the consumption of larger species of fish in which methylmercury is the predominant form (HC, 2007). To a lesser extent, the general population is exposed to inorganic mercury from sources such as dental amalgams (HC, 1996; 2004; SCENIHR 2015). The general population may also be exposed to elemental mercury via inhalation of vapours in ambient air, ingestion or dental and medical treatments (ATSDR, 1999). Methylmercury exposure can occur in utero via cord blood, and it can be transferred to infants through breast milk (ECCC, 2016).

Approximately 95% of methylmercury is absorbed from the gastrointestinal tract following oral ingestion (ATSDR, 1999; 2013). Following absorption, organic mercury is distributed to all tissues, including hair, with highest accumulation in the kidneys. Methylmercury readily passes through the blood-brain barrier and enters the brain, and in pregnant women, it can easily cross the placental barrier into the fetus (ECCC, 2016; HC, 2004). Absorbed organic mercury is demethylated in the body to inorganic mercury that accumulates primarily in the liver and kidneys. The biological half-life of methylmercury in blood has been reported to range between 42 and 70 days in humans (ECCC, 2016). The majority of mercury in the body is excreted via feces, with a small amount excreted as inorganic mercury in urine (ATSDR, 1999; 2013; ECCC, 2016).

Generally, less than 10% of inorganic mercury is absorbed through the intestinal tract (HC, 2004). Absorbed inorganic mercury accumulates readily in the kidneys (IPCS, 2003). It also accumulates in placental tissues, but does not cross placental or blood-brain barriers as easily as elemental or methylmercury (HC, 2004). Excretion of elemental and inorganic mercury compounds occurs mainly in urine and feces, with an absorbed dose half-life of approximately 1 to 2 months (IPCS, 2003).

Elemental mercury is absorbed across the lungs and gastrointestinal tract, with absorption rates of about 80% and 0.01%, respectively (HC, 2004). Once absorbed, elemental mercury enters the bloodstream and is rapidly transported to other parts of the body, including the brain and kidneys. As with organic mercury, it readily crosses the blood-brain and placental barriers (HC, 2004). Once in the body, elemental mercury is oxidized in the tissues to inorganic forms and can remain for weeks or months, with an estimated half-life of approximately 60 days (Sandborgh-Englund et al., 1998).

Long-term exposure to elemental and inorganic mercury is commonly evaluated using mercury concentrations in urine (IPCS, 2003). Hair may also be used as a biomarker of chronic exposure, although inorganic forms of mercury are not excreted in any significant amount in scalp hair, making it an inappropriate biomarker of inorganic mercury exposure (ATSDR, 1999; 2013; IPCS, 2003). Total blood mercury concentrations primarily reflect recent dietary exposure to organic forms of mercury, particularly methylmercury (ATSDR, 1999; 2013; IPCS, 2003). The concentration of total mercury in blood is accepted as a reasonable measure of methylmercury exposure; however, methylmercury itself may also be measured directly in blood. Based on a review of existing data from a number of western countries, the World Health Organization (WHO) has estimated that the average total blood mercury concentration for the general population is approximately 8 µg/L (WHO, 1990). In individuals who consume fish daily, methylmercury concentrations in blood can be as high as 200 µg/L (WHO, 1990).

Mercury is known to be toxic to humans, with the effects depending on the chemical form, the route of exposure, the timing and duration of exposure, and the absorbed concentration. Chronic exposure to low levels of methylmercury through ingestion may not result in any observable symptoms (HC, 2007). The primary effects associated with oral exposure to organic mercury compounds are neurological effects and developmental neurotoxicity (ATSDR, 2013; EFSA CONTAM Panel, 2012; FAO/WHO, 2011; HC, 2007). Symptoms of organic mercury toxicity include a tingling sensation in the extremities; impaired peripheral vision, hearing, taste and smell; slurred speech; muscle weakness and an unsteady gait; irritability; memory loss; depression; and sleeping difficulties. Exposure of a fetus or young child to organic mercury can affect the development of the nervous system, resulting in effects on fine-motor function, attention, verbal learning and memory (ATSDR, 2013; HC, 2007). Exposure to elemental mercury may be hazardous, depending upon the levels of exposure, because the vapour that can be released from this form is readily absorbed into the body through inhalation. Inhalation of mercury vapour may cause respiratory, cardiovascular, kidney and neurological effects. In 1996, Health Canada concluded that mercury exposure from dental amalgams does not pose a health impact for the general population (HC, 1996). Most published studies since this report have concurred that exposure to inorganic mercury from dental amalgams has not been associated with neurologic effects in children or adults (Bates et al., 2004; Bellinger et al., 2007; DeRouen et al., 2006; Factor-Litvak et al., 2003; SCENIHR, 2015).

The International Agency for Research on Cancer (IARC) determined that methylmercury compounds are possibly carcinogenic to humans (Group 2B), based on animal data showing a link to certain cancers, particularly renal cancer (IARC, 1993). IARC has determined that elemental mercury and inorganic mercury compounds are not classifiable as to their carcinogenicity to humans (Group 3) (IARC, 1993).

The United Nations Environment Programme (UNEP) Global Mercury Assessment has concluded that there is sufficient evidence of adverse impacts from mercury to warrant international action to reduce the risks to human health and the environment (UNEP, 2013). International negotiations under UNEP resulted in the signing of the Minamata Convention on Mercury, a global legally binding agreement to prevent mercury emissions and releases (UNEP, 2019). The Minamata Convention is intended to reduce global atmospheric emissions, supply, trade and demand for mercury, and to find environmentally sound solutions for storage of mercury and mercury-containing wastes. It also supports a gradual phase-down of the use of dental amalgam in restorative treatment.

In Canada, mercury and its compounds are listed as toxic substances on Schedule 1 of the Canadian Environmental Protection Act, 1999 (Canada, 1999; Canada, 2012). Existing and planned actions to manage the risks from mercury are summarized in the Government of Canada's Risk Management Strategy for Mercury (EC and HC, 2010). These risk management actions include several Canada-wide standards that have been established to reduce releases of mercury to the environment (Canada, 2013). The Products Containing Mercury Regulations came into force in 2015 and prohibit the manufacture and import of products containing mercury or any of its compounds, as well as provide content limits for exempted products (Canada, 2014). The Surface Coating Materials Regulations, in effect under the Canada Consumer Product Safety Act, restrict the level of mercury in all surface coating materials advertised, sold or imported into Canada (Canada, 2005). In addition, the Toys Regulations prohibit any compound of mercury in the surface coating material that is applied to a product used by a child in learning or play situations (Canada, 2011). Mercury and its compounds are on the List of Ingredients that are Prohibited for Use in Cosmetic Products (HC, 2019a). The Food and Drug Regulations prohibit the sale in Canada of drugs for human use containing mercury or any of its salts or derivatives except in some specific instances, including those where it is present as a preservative (Canada, 1978).

Health Canada has established a methylmercury blood guidance value of 20 µg/L for the general adult population; a methylmercury concentration in blood below this value is considered within the normal acceptable range (HC, 2004). For children (under 18 years), pregnant women, and women of child-bearing age (under 50 years), a provisional methylmercury blood guidance value of 8 µg/L has been proposed (Legrand et al., 2010). On the basis of health considerations, Health Canada, in collaboration with the Federal-Provincial-Territorial Committee on Drinking Water, has developed a guideline for Canadian drinking water quality that establishes the maximum acceptable concentration for mercury in drinking water (HC, 1986). Health Canada has also established maximum levels for mercury in retail fish (HC, 2020b) and provides consumption advice for consumers of certain types of fish (HC, 2019b). Mercury was analyzed as part of Health Canada's ongoing Total Diet Study surveys (Dabeka et al., 2003; HC, 2020a). The food items analyzed represent those that are most typical of the Canadian diet. These surveys are used to provide dietary exposure estimates for chemicals to which Canadians in different age-sex groups are exposed through the food supply.

Mercury concentrations in blood have been measured in a number of biomonitoring studies conducted in Canada, including the Maternal–Infant Research on Environmental Chemicals study (Arbuckle et al., 2016) and the First Nations Biomonitoring Initiative (AFN, 2013).

Total mercury was analyzed in the whole blood of CHMS participants aged 6–79 in cycle 1 (2007–2009) and aged 3–79 in cycle 2 (2009–2011), cycle 3 (2012–2013), cycle 4 (2014–2015), cycle 5 (2016–2017) and cycle 6 (2018–2019). Methylmercury was analyzed in the whole blood of CHMS participants aged 20–79 in cycles 3 and 4, and aged 3–19 in cycles 5 and 6. Inorganic mercury was analyzed in the whole blood of CHMS participants aged 6–79 in cycle 1 and aged 3–19 in cycles 5 and 6. Data from these cycles are presented in blood as µg/L. In addition, inorganic mercury was analyzed in the urine of CHMS participants aged 6–79 in cycle 1 and aged 3–79 in cycles 3 and 4, and total mercury was analyzed in hair from CHMS participants aged 20–59 in cycle 5. Finding a measurable amount of mercury in blood, urine or hair is an indicator of exposure to mercury and does not necessarily mean that an adverse health effect will occur.

References

• AFN (Assembly of First Nations) (2013). First Nations Biomonitoring Initiative: National Results (2011). Assembly of First Nations, Ottawa, ON. Retrieved February 2, 2021.
• Arbuckle, T.E., Liang, C.L., Morisset, A.S., Fisher, M., Weiler, H., Cirtiu, C.M., Legrand, M., Davis, K., Ettinger, A.S., Fraser, W.D., et al. (2016). Maternal and fetal exposure to cadmium, lead, manganese and mercury: The MIREC study. Chemosphere, 163, 270–282.
• ATSDR (Agency for Toxic Substances and Disease Registry) (1999). Toxicological Profile for Mercury. U.S. Department of Health and Human Services, Atlanta, GA. Retrieved February 24, 2021.
• ATSDR (Agency for Toxic Substances and Disease Registry) (2013). Addendum to the Toxicological Profile for Mercury (Alkyl and Dialkyl Compounds). U.S. Department of Health and Human Services, Atlanta, GA. Retrieved February 24, 2021.
• Bates, M.N., Fawcett, J., Garrett, N., Cutress, T., and Kjellstrom, T. (2004). Health effects of dental amalgam exposure: A retrospective cohort study. International Journal of Epidemiology, 33(4), 894–902.
• Bellinger, D.C., Daniel, D., Trachtenberg, F., Tavares, M., and McKinlay, S. (2007). Dental amalgam restorations and children's neuropsychological function: The New England Children's Amalgam Trial. Environmental Health Perspectives, 115(3), 440–446.
• Canada (1978). Food and Drug Regulations. C.R.C., c. 870. Retrieved February 24, 2021.
• Canada (1999). Canadian Environmental Protection Act, 1999. SC 1999, c. 33. Retrieved February 24, 2021.
• Canada (2005). Surface Coating Materials Regulations. SOR/2005-109. Retrieved February 24, 2021.
• Canada (2011). Toys Regulations. SOR/2011-17. Retrieved February 24, 2021.
• Canada (2012). Order Adding Toxic Substances to Schedule 1 to the Canadian Environmental Protection Act, 1999. Canada Gazette, Part II: Official Regulations, 146(21). Retrieved February 24, 2021.
• Canada (2013). Mercury: Canada-wide standards. Retrieved June 4, 2021. 
• Canada (2014). Products Containing Mercury Regulations. SOR/2014-254. Retrieved February 24, 2021.
• Dabeka, R.W., McKenzie, A.D., and Bradley, P. (2003). Food Additives and Contaminants, 20, 629-638.
• DeRouen, T.A., Martin, M.D., Leroux, B.G., Townes, B.D., Woods, J.S., Leitão, J., Castro-Caldas, A., Luis, H., Bernardo, M., Rosenbaum, G., et al. (2006). Neurobehavioral effects of dental amalgam in children: A randomized clinical trial. Journal of the American Medical Association, 295(15), 1784–1792.
• EFSA CONTAM Panel (European Food Safety Authority Panel on Contaminants in the Food Chain) (2012). Scientific opinion on the risk for public health related to the presence of mercury and methylmercury in food. European Food Safety Authority Journal, 10(12), 2985.
• ECCC (Environment and Climate Change Canada) (2016). Mercury and human health (Chapter 14), Canadian Mercury Science Assessment Report. Minister of Environment and Climate Change, Ottawa, ON. Retrieved February 24, 2021.
• ECCC (Environment and Climate Change Canada) (2017). Mercury and the environment. Minister of Environment and Climate Change, Ottawa, ON. Retrieved February 24, 2021.
• EC and HC (Environment Canada and Health Canada) (2010). Risk Management Strategy for Mercury. Minister of the Environment, Ottawa, ON. Retrieved February 24, 2021.
• Factor-Litvak, P., Hasselgren, G., Jocobs, D., Begg, M., Kline, J., Geier, J., Mervish, N., Schoenholtz, S., and Graziano, J. (2003). Mercury derived from dental amalgams and neuropsychologic function. Environmental Health Perspectives, 111(5), 719–723.
• FAO/WHO (Food and Agriculture Organization of the United Nations/World Health Organization) (2011). Mercury (addendum). Safety evaluation of certain contaminants in food. Seventy-second meeting of the Joint FAO/WHO Expert Committee on Food Additives, World Health Organization, Geneva. Retrieved February 24, 2021.
• HC (Health Canada) (1986). Guidelines for Canadian Drinking Water Quality: Guideline Technical Document – Mercury. Minister of Health, Ottawa, ON. Retrieved February 23, 2021.
• HC (Health Canada) (1996). The Safety of Dental Amalgam. Minister of Health, Ottawa, ON. Retrieved February 23, 2021.
• HC (Health Canada) (2004). Mercury: Your Health and the Environment: A Resource Tool. Minister of Health, Ottawa, ON. Retrieved February 23, 2021.
• HC (Health Canada) (2007). Human Health Risk Assessment of Mercury in Fish and Health Benefits of Fish Consumption. Minister of Health, Ottawa, ON. Retrieved February 23, 2021.
• HC (Health Canada) (2019a). List of Ingredients that are Prohibited for Use in Cosmetic Products (Hotlist). Minister of Health, Ottawa, ON. Retrieved February 23, 2021.
• HC (Health Canada) (2019b). Mercury In Fish – Consumption Advice: Making Informed Choices About Fish. Minister of Health, Ottawa, ON. Retrieved February 23, 2021.
• HC (Health Canada) (2020a). Canadian Total Diet Study. Minister of Health, Ottawa, ON. Retrieved February 23, 2021.
• HC (Health Canada) (2020b). Health Canada's Maximum Levels for Chemical Contaminants in Foods. Minister of Health, Ottawa, ON. Retrieved February 23, 2021.
• IARC (International Agency for Research on Cancer) (1993). IARC Monographs on the Evaluation of Carcinogenic Risks to Humans – Volume 58: Beryllium, Cadmium, Mercury, and Exposures in the Glass Manufacturing Industry. World Health Organization, Lyon. Retrieved February 24, 2021.
• IMERC (Interstate Mercury Education and Reduction Clearinghouse) (2010). Fact sheet – Mercury Use in Dental Amalgam. Northeast Waste Management Officials' Association, Boston, MA. Retrieved February 24, 2021.
• IPCS (International Programme on Chemical Safety) (2003). Concise International Chemical Assessment Document 50 – Elemental Mercury and Inorganic Mercury Compounds: Human Health Aspects. World Health Organization, Geneva. Retrieved February 24, 2021.
• Legrand, M., Feeley, M., Tikhonov, C., Schoen, D., and Li-Muller, A. (2010). Methylmercury blood guidance values for Canada. Canadian Journal of Public Health, 101(1), 28–31.
• Richardson, G.M. (2014). Mercury exposure and risks from dental amalgam in Canada: The Canadian Health Measures Survey 2007–2009. Human and Ecological Risk Assessment: An International Journal, 20(2), 433–447.
• Sandborgh-Englund, G., Elinder, C., Johanson, G., Lind, B., Skare, I., and Ekstrand, J. (1998). The absorption, blood levels, and excretion of mercury after a single dose of mercury vapor in humans. Toxicology and Applied Pharmacology, 150(1), 146–153.
• SCENIHR (Scientific Committee on Emerging and Newly Identified Health Risks) (2015). Opinion on the safety of dental amalgam and alternative dental restoration materials for patients and users. European Commission, DG Health and Food Safety, Luxembourg. Retrieved February 24, 2021.
• UNEP (United Nations Environment Programme) (2013). Global Mercury Assessment 2013: Sources, Emissions, Releases, and Environmental Transport. UNEP Chemicals Branch, Geneva. Retrieved February 24, 2021.
• UNEP (United Nations Environment Programme) (2019). Minamata Convention on Mercury. United Nations. Retrieved February 24, 2021.
• WHO (World Health Organization) (1990). Environmental Health Criteria 101: Methylmercury. WHO, Geneva. Retrieved February 24, 2021.

8.7 Selenium

Selenium (CASRN 7782-49-2) is a naturally occurring trace mineral distributed widely in the environment (Schamberger, 1984). Selenium is present in the environment in the inorganic form as selenide, selenate and selenite, but rarely as elemental selenium. Selenium is an essential trace element required for the maintenance of good health in humans.

Selenium in its organic form is found in trace quantities in most plants and animal tissues (Schamberger, 1984). Elevated levels of selenium in the environment may occur naturally from weathering of base-metal deposits and soils (CCME, 2009). Selenium is also released into the environment as a result of anthropogenic activities, such as mining or metallurgical processes (CCME, 2009). Other sources of anthropogenic selenium emissions include incinerator stacks, burning coal and oil, and large-scale combustion processes.

Historically, selenium was primarily used in the electronics industry in the form of arsenic triselenide, a photoreceptor for photocopiers (USGS, 2001). Because selenium has various electrical and conductive properties, it is also used in light meters, photoelectric and solar cells, semiconductors and arc-light electrodes. It is also used as a colourizing and decolourizing agent for glass, and to reduce solar heat for architectural glass (USGS, 2004). Selenium is also present in stainless steel, enamels, inks, rubber, batteries, explosives, fertilizers, animal feed, pharmaceuticals and shampoos (ATSDR, 2003).

The Canadian population is exposed to selenium compounds in food, ambient air, drinking water, soil and natural health products. More than 99% of the total daily intake of selenium is estimated to occur through the diet for the general population and all age groups (CCME, 2009). Absorption of selenium depends on the chemical form; organic forms are absorbed more readily (>90%) than inorganic forms (>50%) (IOM, 2000). Absorption also depends on the overall exposure level; absorption increases when selenium levels in the body are low (IOM, 2000). Once inside the body, selenium generally concentrates in the liver and kidneys regardless of the initial chemical form. It can also be found in nails and hair (IOM, 2000). Selenium elimination is triphasic, with biological half-lives of approximately 1 day, 1 week and 3 months (ATSDR, 2003). Approximately 50% to 80% of absorbed selenium is eliminated in the urine (Marier and Jaworski, 1983). Selenium levels in the body following both short- and long-term exposure can be determined through blood and urine tests (IOM, 2000). Human breath can also be used as a biomarker for selenium exposure when large amounts of selenium are being excreted (IOM, 2000).

Selenium is an essential trace element and a component of several proteins and enzymes in the body (ATSDR, 2003; HC, 2010). Selenium aids in the defence of oxidative stress, the regulation of thyroid hormone action, and the regulation of the redox status of vitamin C and other molecules (IOM, 2000). Selenium deficiency seldom causes overt illness in isolation; however, it may lead to biochemical changes that predispose people to illness associated with other stresses (IOM, 2000). There is some evidence that suboptimal levels of selenium may lead to sperm abnormalities and effects on sperm motility (Ahsan et al., 2014). On account of its essentiality, Health Canada has established recommended dietary allowances for selenium (HC, 2010; IOM, 2000).

There is a narrow therapeutic window for selenium, and adverse health effects can occur when ingested at levels greater than the tolerable upper intake level (HC, 2010; IOM, 2000). The level at which selenium toxicity occurs can be difficult to determine because it is affected by the types of protein in the diet, levels of vitamin E, and the forms of selenium to which the individual is exposed (HC, 2014). Acute oral intake of excess selenium can result in nausea, vomiting and diarrhea. Selenosis, a disease that results in hair loss, nail brittleness and neurological abnormalities, is the critical health effect associated with chronic exposure to elevated levels of selenium (i.e., 10 to 20 times more than the recommended dietary allowances) (ATSDR, 2003; IOM, 2000; WHO, 2011). The role of selenium in other chronic diseases, such as diabetes, hypertension and cardiovascular disease, is a subject of ongoing investigation (Benstoem et al., 2015; Boosalis, 2008; Ogawa-Wong et al., 2016). The International Agency for Research on Cancer has determined that selenium's carcinogenicity to humans is not classifiable (Group 3) (IARC, 1975).

The Government of Canada conducted a science-based screening assessment under the Chemicals Management Plan to determine whether selenium and its compounds (including 29 selenium-containing substances on the Domestic Substances List) present or may present a risk to the environment or human health as per the criteria set out in section 64 of the Canadian Environmental Protection Act, 1999 (CEPA 1999) (Canada, 1999; ECCC and HC, 2017a). The assessment concluded that selenium and its compounds are toxic under CEPA 1999 as they are harmful to human health — based on the potential for elevated levels in certain Canadian subpopulations that have higher intake — as well as being harmful to the environment. Selenium and its compounds are proposed to be added to Schedule 1, List of Toxic Substances, under CEPA 1999 (Canada, 1999; HC, 2020b). Risk management actions for selenium and its compounds have been proposed that include measures to reduce the release of selenium into water and finalizing the revised maximum daily dose allowed for selenium in natural health products (ECCC and HC, 2017b). Selenium and its compounds (except selenium sulfide) are on the List of Ingredients that are Prohibited for Use in Cosmetic Products (HC, 2019).

In Canada, the leachable selenium content in a variety of consumer products is regulated under the Canada Consumer Product Safety Act (Canada, 2010a). Consumer products regulated for selenium content include paints and other surface coatings on cribs, toys and other products for use by a child in learning or play situations (Canada, 2010b; Canada, 2011). Health Canada has also set a maximum level for selenium in natural health products in Canada (HC, 2018). Health Canada has developed a Canadian drinking water quality guideline that sets out the maximum acceptable concentration of selenium on the basis of health considerations (HC, 2014). Tolerable upper intake levels for selenium, which account for its potential toxicity, have been developed by the Institute of Medicine and adopted by Health Canada (HC, 2010; IOM, 2000). Selenium is also included in the list of various chemicals analyzed as part of Health Canada's ongoing Total Diet Study surveys (HC, 2020a). These surveys provide estimates of the levels of chemicals to which Canadians in different age-sex groups are exposed through the food supply.

Selenium concentrations in blood have been measured in a limited number of biomonitoring studies conducted in Canada, including the First Nations Biomonitoring Initiative (AFN, 2013).

Selenium was measured in the whole blood of Canadian Health Measures Survey (CHMS) participants aged 6–79 in cycle 1 (2007–2009), and aged 3–79 in cycle 2 (2009–2011), cycle 5 (2016–2017) and cycle 6 (2018–2019). Data from these cycles are presented in blood as µg/L. Selenium was also measured in the urine of all CHMS participants aged 6–79 in cycle 1 and aged 3–79 in cycle 2, and was analyzed in hair from participants aged 20–59 in cycle 5. Finding a measurable amount of selenium in blood, urine or hair is an indicator of exposure to selenium and does not necessarily mean that an adverse health effect will occur. Because selenium is an essential trace element, its presence in biological fluids is expected.

References

• AFN (Assembly of First Nations) (2013). First Nations Biomonitoring Initiative: National Results (2011). Assembly of First Nations, Ottawa, ON. Retrieved February 2, 2021.
• Ahsan, U., Kamran, Z., Raza, I., Ahmad, S., Babar, W., Riaz, M.H., and Iqbal, Z. (2014). Role of selenium in male reproduction – a review. Animal Reproduction Science, 146, (1–2), 55–62.
• ATSDR (Agency for Toxic Substances and Disease Registry) (2003). Toxicological Profile for Selenium. U.S. Department of Health and Human Services, Atlanta, GA. Retrieved March 1, 2021.
• Benstoem, C., Goetzenich, A., Kraemer, S., Borosch, S., Manzanares, W., Hardy, G., and Stoppe, C. (2015). Selenium and Its Supplementation in Cardiovascular Disease—What do We Know? Nutrients, 7(5), 3094–3118.
• Boosalis, M.G. (2008). The role of selenium in chronic disease. Nutrition in Clinical Practice, 23 (2), 152–160.
• Canada (1999). Canadian Environmental Protection Act, 1999. SC 1999, c. 33. Retrieved March 1, 2021.
• Canada (2010a). Canada Consumer Product Safety Act. SC 2010, c. 21. Retrieved March 1, 2021.
• Canada (2010b). Cribs, Cradles and Bassinets Regulations. SOR/2010-261. Retrieved March 1, 2021.
• Canada (2011). Toys Regulations. SOR/2011-17. Retrieved March 1, 2021.
• CCME (Canadian Council of Ministers of the Environment) (2009). Canadian Soil Quality Guidelines for the Protection of Environmental and Human Health – Selenium. Winnipeg, MB. Retrieved July 12, 2021.
• ECCC and HC (Environment and Climate Change Canada and Health Canada) (2017a). Final screening assessment: Selenium and its compounds. Minister of Environment and Climate Change, Ottawa, ON. Retrieved March 1, 2021.
• ECCC and HC (Environment and Climate Change Canada and Health Canada) (2017b). Risk Management Approach for Selenium and its Compounds under the Selenium-containing Substance Grouping. Minister of Environment and Climate Change, Ottawa, ON. Retrieved March 1, 2021.
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