Proposal - Maximum Chemical Contaminant Levels in Livestock Feeds

August 2017

Purpose

The Canadian Food Inspection Agency (CFIA) has embarked on a comprehensive change agenda to strengthen its foundation of legislation, regulatory programs and inspection approaches and tools. These directions set the context for the renewal of the federal Feeds Regulations (Regulations).

The goal of renewing the Regulations is to develop a modernized risk- and outcome-based regulatory framework for feeds which:

  • safeguards feeds and the food production continuum;
  • attains the most effective and efficient balance between fair and competitive trade in the market; and
  • minimizes regulatory burden.

Modernization of the Regulations provides the opportunity to review feed controls, standards, labelling, and other regulatory requirements. The purpose of this proposal is to review the current standards for dioxins, furans, PCBs, metals and other chemical contaminants to identify updates or amendments to the current requirements, if applicable. Currently maximum standards for contaminants dealt with in this proposal are found in the current Feed Regulations or in regulatory guidance (RG-8).

Given the considerations outlined below, the CFIA is aiming to provide a science-based, enforceable list of maximum levels of some known chemical contaminants in feeds that can be updated in a timely manner as needed to reflect changing risks and science.

Background and Current Situation

The CFIA verifies that livestock feeds manufactured, sold in, and imported into Canada are safe, effective and labelled appropriately to contribute to the production and maintenance of healthy livestock and safe foods of animal origin. The CFIA confirms regulatory compliance by a variety of inspection activities including pre-market assessments and post-market inspection activities (e.g., product sampling and testing) to verify compliance with standards and to monitor for the presence of known chemical contaminants.

Section 19(1) of the Regulations also states:

Subject to subsections (2) and (3), a feed shall not contain…

(j) any material in quantities that could, when fed in proportions commonly used or as specified in the feeding directions, result in the production of an article of food that is prohibited from sale by virtue of section 4 of the Food and Drugs Act; or

(k) any material, other than those referred to in paragraphs (a) to (j), in quantities likely to be deleterious to livestock, when fed in proportions commonly used or as specified in the feeding directions.

To provide greater clarity to stakeholders regarding standards for those contaminants not specifically identified in the Regulations, the CFIA provides guidance in the form of action levels for additional contaminants, e.g., dioxins and heavy metals, in the publication RG-8 Regulatory Guidance: Contaminants in Feed.

Considerations

Livestock feed and feed ingredients can act as a route of entry for hazards into human food and for hazards that pose a risk to animal health, and/or the environment (e.g., non-target organisms). Some examples are:

Dioxins, Furans and PCBs

  • Dioxins, furans and PCBs are persistent environmental contaminants and bioaccumulate in the food chain. Scientific literature has shown that these contaminants have the potential to cause a variety of adverse effects to animals and humans.
  • It has been estimated that the major source (approximately 90 percent) of human exposure to dioxins, furans, and PCBs is from foods of animal origin. It has been further estimated that 80 percent of these contaminants in foods of animal origin originate from livestock feeds.
  • Standards have been established for feed ingredients which are known to be sources of these contaminants (e.g., mineral-based ingredients, fish meal, fish oil, etc.).
  • CFIA is aligned with national and international jurisdictions to continually reduce these contaminants from entering the feed and food chains by setting and enforcing standards for them in feed ingredients.

Metals and Trace Element Contaminants

  • Metals and trace elements are inorganic substances found in the Earth's crust. Many are essential for health and productivity of livestock and have well-defined nutritional and biochemical roles.
  • Many others naturally occur at trace levels in food and tissues of animals, but are not typically suspected to play a useful nutritional purpose and are considered incidental contaminants including heavy metals such as arsenic, cadmium, and lead.
  • Whether essential or nonessential metals and trace elements can adversely affect an animal when amounts in the diet and/or water become excessive.
  • Furthermore, metals and trace elements can be transferred to the human food chain through consumption of foods of animal origin, and feeds with high metal loads pose a human health hazard to those individuals working with, or otherwise exposed to, the product.
  • Some heavy metal and trace element contaminants of concern are arsenic, cadmium, lead and fluorine.

As outlined in the CFIA's 2014 Feed Hazard Identification / Preventive Controls Regulatory Framework Proposal, all parties throughout the feed supply chain to whom the regulatory framework would apply would be required to:

  • identify hazards that may be associated with their products and processes; and,
  • design and implement a Preventative Control Plan (PCP) to address the identified hazards that are appropriate for their specific system.

This proposal went on to say, "To modernize the current regulatory framework regarding the identification of hazards, the Agency proposes to:

  • revise the list of specific hazards and standards identified for feeds, as appropriate;
  • identify specific hazards and maximum levels in feeds in guidance (build on current RG-8); and,
  • include known hazards and levels, where appropriate, in ingredient descriptions set out in Schedule IV of the Regulations."

Scope of the Reviews

Current standards and action levels, as well as scientific literature, were reviewed to guide the establishment of a regulatory standard. The standard is based on the assessment of the impacts of the chemical contaminants on animal health and production, human health, including food safety and worker/by-stander exposure, and the environment.

Information sources used in these reviews included:

Proposal

Given the potential negative impacts described above associated with the presence of dioxins, furans, PCBs, metals and trace elements in livestock feeds, there remains a continued need for an enforceable regulatory framework in a modernized regulation. Therefore, it is proposed that:

  • Maximum levels will be established in the Regulations for livestock feed ingredient(s) and/or total livestock diet(s), as applicable, for the following chemical contaminants:
    • dioxins, furans, and dioxin-like PCBs;
    • total PCBs;
    • metal contaminants (i.e., the heavy metals lead, cadmium, arsenic); and,
    • fluorine.

It is further proposed that these maximum levels would be incorporated by reference in the Regulations, thus providing greater flexibility in amending the standards and proposing additional standards as scientific knowledge and evidence advance. Incorporation of documents by reference is a drafting technique that brings the content of a document into a regulation, without the need to reproduce the document in the regulation itself. The CFIA has developed the Incorporation by Reference Policy to articulate a clear and comprehensive process for identifying documents that could be incorporated by reference.

Appendix I is the proposed maximum levels and associated rationales for these contaminants in livestock feeds and/or feed ingredients.

Appendix II includes additional technical material for each chemical contaminant.

These standards would apply to feeds manufactured or imported for domestic use. In addition, and as outlined in the CFIA's 2015 Consolidated Modernized Framework Proposal, all feeds manufactured in Canada intended for export would need to meet Canadian standards for safety and other domestic compliance requirements. Feeds for export or feeds manufactured to be compliant with food export programs may be subject to additional importing country or export program requirements.

Anticipated Outcomes

This modernized regulatory approach to setting maximum levels for chemical contaminants in a document incorporated by reference in the Regulations will:

  • allow the CFIA to maintain regulatory oversight for hazards that may negatively impact human health, animal health and/or the environment;
  • provide stakeholders with clear standards, referenced in the Regulations, for identified hazards;
  • allow for timely updates to the standards as new information for specific chemical contaminants are provided;
  • harmonize, to the extent possible, with other jurisdictions such as the U.S. and European Union; and,
  • assure that domestic feeds and those in international trade originating from Canada are as safe as possible.

It is important to note that while maximum levels are being proposed for specific chemical contaminants, this is not an exhaustive list and other contaminants will be discussed in other proposals. Feed manufacturers are reminded of their responsibility to produce feeds which are safe for all classes of livestock species and to prevent the introduction of chemical contaminants into the food chain via foods of animal origin. The identification of specific contaminants which, represent a hazard if not adequately controlled, is critical for the development of preventative control plans.

References: A complete bibliography is available upon request.

Have your say

The CFIA is seeking feedback on the proposal to modify the regulatory requirements related to chemical contaminant standards in livestock feed:

  • Do you have any concerns with the proposal to establish maximum contaminant levels in the Regulations for livestock feeds?
  • Do you have any concerns with the identified contaminants and proposed maximum values outlined in Appendix I?
  • Is there valid scientific information that has not been considered?
  • Would the proposed amendments to the Feeds Regulations be effective in protecting human and animal health and the environment?
  • Are there options not mentioned in this proposal that should be explored?
  • Any additional feedback?

We strongly encourage you to provide your input and feedback, which is critically important to the success of the regulatory modernization initiative. Written comments may be forwarded by September 22, 2017 to:

Sergio Tolusso
Canadian Food Inspection Agency
Animal Feed Division
59 Camelot Drive
Ottawa, ON K1A 0Y9
Email: Sergio.tolusso@inspection.gc.ca
Fax: 613-773-7565

Appendix I – Proposed Maximum Contaminant Levels in Total Livestock Diets and/or Feed Ingredients

Maximum Levels for Dioxins, Furans, and Dioxin-Like PCBs Table Note 1
Livestock Feed Ingredient Proposed Maximum
Level Table Note 2
(ng WHO-TEQ2005/kg)
Current Action
Level Table Note 3
(ng WHO-TEQ2005/kg)
Fish Meal 2.5 3.0
Fish Oil 12 16

Single Mineral Feed Ingredients (e.g., Copper Sulphate, Zinc Oxide)

Mineral Complexes; Mineral Chelates; Mineral Proteinates

Trace Mineral Micro-Premixes

1 1.5
Anti-Caking Agents 1.5 1.5

Vegetable Oils and By-Products of Vegetable Oil Manufacturing

For example:

  • Vegetable (palm) oil
  • Hydrogenated vegetable (palm) oil
  • Calcium salts of fatty acids
  • Fractionated palm fatty acid distillates
  • Hydrogenated palm fatty acid distillates
  • Palm palmitic acid (C16:0)

0.75 (dioxins and furans only)

1.5 (dioxins, furans and dioxin-like PCBs)

0.75 (dioxins and furans only)

1.5 (dioxins, furans and dioxin-like PCBs)

Table Notes

Table Note 1

Referring to seven (7) dioxin congeners, ten (10) furan congeners and twelve (12) dioxin-like PCB congeners (see Appendix II).

Return to table note 1 referrer

Table Note 2

Maximum levels are based on total weight; not moisture or fat corrected values.

Return to table note 2 referrer

Table Note 3

RG-8 Regulatory Guidance: Contaminants in Feeds

Return to table note 3 referrer

Rationale:

  • These standards align with guidance set by other international agencies with the approach to continually prevent and reduce these contaminants from entering the feed and food chains.
  • Feed monitoring data collected by the CFIA from 2007 to 2016 under the National Feed Inspection Program were analyzed.
  • The maximum levels for dioxins and DL-PCBs were calculated by adding two standard deviations to the mean concentration in samples of each ingredient type. The resulting values were then rounded to the nearest 0.5 ng WHO-TEQ/kg.
  • The maximum levels for dioxins and furans, with or without DL-PCBs in vegetable oils and by-products of vegetable oil manufacturing align with levels established by the European Commission.
Maximum Level for Total PCBs in Marine Oils
Livestock Feed Ingredient Proposed Maximum
Level Table Note 4
(mg/kg)
Current Action
Level Table Note 5
(mg/kg)

Marine Oils (oils from approved marine sources listed in Schedule IV)

For example:

  • Fish oil
  • Mollusc oil
0.3 0.3

Table Notes

Table Note 4

Maximum levels are based on total weight.

Return to table note 4 referrer

Table Note 5

RG-8 Regulatory Guidance: Contaminants in Feeds

Return to table note 5 referrer

Rationale:

  • The maximum total PCB level in marine oils for use as livestock feed ingredients was calculated based on sample monitoring data collected from 2000 to 2006, by adding one standard deviation to the mean and rounding the resulting value to the nearest 0.1 mg/kg.
Maximum Levels for Arsenic in Total Diets of Livestock
Total Livestock Diet Proposed Maximum
Level
(mg/kg)
Current Action
Level Table Note 6
(mg/kg)

Total diet Table Note 7 for all livestock species

8 8

Table Notes

Table Note 6

RG-8 Regulatory Guidance: Contaminants in Feeds

Return to table note 6 referrer

Table Note 7

Total diet refers to the complete feed for monogastric livestock species and considers complete feed and forage for horses and ruminants.

Return to table note 7 referrer

Rationale:

  • Based on the review of the scientific information, standards set by other national and international jurisdictions, and sample monitoring data, the current maximum level for arsenic in feed is sufficient to mitigate the risk of arsenic toxicity to animal health and human health including transfer to foods of animal origin.
  • Analysis of sampling data indicates that currently available ingredients, when used for their intended purpose (e.g., macro and trace mineral sources), meet this standard therefore product availability is unlikely to be impacted.
Maximum Levels for Cadmium in Total Diets of Livestock
Total Livestock Diet Proposed Maximum
Level
(mg/kg)
Current Action
Level Table Note 8
(mg/kg)

Total diet Table Note 9 for horses

0.2 0.2
Total diet for all other livestock species 0.4 0.4

Table Notes

Table Note 8

RG-8 Regulatory Guidance: Contaminants in Feeds

Return to table note 8 referrer

Table Note 9

Total diet refers to the complete feed for monogastric livestock species and considers complete feed and forage for horses and ruminants.

Return to table note 9 referrer

Rationale:

  • Based on the scientific data and other relevant information (related to the toxicity of cadmium to animal and human health) as well as sample monitoring data for cadmium in feed, the current maximum levels of cadmium will remain unchanged.
  • Analysis of sampling data indicates that currently available ingredients, when used for their intended purpose (e.g., macro and trace mineral sources), meet this standard therefore product availability is unlikely to be impacted.
Maximum Levels for Lead in Total Diets of Livestock
Total Livestock Diet Proposed Maximum
Level
(mg/kg)
Current Action
Level Table Note 10
(mg/kg)

Total diet Table Note 11 for all livestock species

8 8

Table Notes

Table Note 10

RG-8 Regulatory Guidance: Contaminants in Feeds

Return to table note 10 referrer

Table Note 11

Total diet refers to the complete feed for monogastric livestock species and considers complete feed and forage for horses and ruminants.

Return to table note 11 referrer

Rationale:

  • Based on the scientific data and other relevant information (related to the toxicity of lead to animal and human health) as well as sample monitoring data for lead in feed, the current maximum level of lead will remain unchanged.
Maximum Levels for Fluorine in Livestock Feeds
Feed Type Proposed Maximum
Level
(mg/kg)
Current Regulatory
Maximum Table Note 12
(mg/kg)
Mineral feed for Cattle, Sheep or Horses containing 9% or less of Phosphorus 2,000 2,000
Mineral feed for Cattle, Sheep or Horses containing greater than 9% of Phosphorus 3,000 3,000
Mineral feed for Swine 6,000 6,000
Complete feed for Horse and Rabbits 40 40
Complete feed for Cattle and Sheep 50 50
Complete feed for Swine and Turkeys 150 150
Complete feed for Chickens 200 200
Complete feed for other livestock species 150 N/A (Not applicable)

Table Notes

Table Note 12

Feeds Regulations, 1983, section 19(1)(b)

Return to table note 12 referrer

Rationale:

  • Based on the scientific data and other relevant information (related to the toxicity of fluorine to animal and human health), the current maximum levels of fluorine in mineral feeds and/or complete feeds will remain unchanged.
  • The maximum level of fluorine in complete feed for other livestock species of 150 ppm aligns with the level established by the European Commission as an undesirable substance in animal feed.

Appendix II – Additional Technical Information

Dioxins, Furans and PCBs

Polychlorinated dibenzo-para-dioxins (PCDDs) and dibenzofurans (PCDFs), commonly referred to as dioxins, are persistent organic pollutants (POPs) formed as unwanted by-products of several industrial activities including, metal processing, chlorine bleaching of pulp and paper, waste incineration and the manufacturing of some chlorinated organic compounds. Dioxins can also be produced naturally by forest fires and volcanic eruptions. Due to several regulatory measures, the release of dioxins into the environment from these sources has decreased significantly over the years (European Commission 2000, EFSA 2012).

Dioxins consist of 75 PCDD congeners and 135 PCDF congeners that differ in the degree of chlorination (1-8 chlorine atoms) and chlorine substitution pattern. Seven PCDD congeners and ten PCDF congeners have a chlorine substitution in the 2,3,7,8-position. These 17 congeners are the ones of toxicological concern, with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) being the most toxic dioxin congener (European Commission 2000).

Polychlorinated biphenyls (PCBs) are also classified as POPs. Unlike PCDDs and PCDFs, PCBs were intentionally manufactured for use in products including transformers, insulators and capacitors, until they were banned in the late 1970s. The use of products containing PCBs is currently being phased out. Out of the 209 PCB congeners, 12 congeners are referred to as "dioxin-like PCBs" (DL-PCBs) because of their ability to adopt a coplanar structure, resulting in similar toxicological characteristics to dioxins (European Commission 2000, EFSA 2010, EFSA 2012).

Dioxins and PCBs persist in the environment and bioaccumulate in the food chain because of their lipophilic characteristics and resistance to degradation. As a result, they are ubiquitous in the environment and can be found at very low levels in living organisms. Since dioxins and PCBs accumulate in adipose tissue of animals, there is particular concern for human exposure through the consumption of foods of animal origin (meat, milk products, fish and shellfish). It has been estimated that the majority of human exposure to dioxins and PCBs occurs through the diet, with more than 90 percent being contributed by foods of animal origin. It has also been estimated that 80 percent of these contaminants found in foods of animal origin are thought to originate from contamination in livestock feeds (European Commission 2000, CAC 2006). Therefore, control measures at the feed ingredient level are critical to reducing contamination in foods of animal origin and reducing human exposure.

Exposure to dioxins and DL-PCBs can result in adverse effects on the nervous, endocrine and immune systems, as well as adverse effects on development and reproductive function in animals and humans (JECFA 2002). They have also been shown to cause cancer. The World Health Organization's (WHO) International Agency for Research on Cancer (IARC) has classified 2,3,7,8-TCDD as a Group 1 carcinogen, meaning it is carcinogenic to humans (IARC 1997).

Acceptable methods for quantitative analysis of dioxins and PCBs typically include a clean-up/extraction system (liquid-liquid extraction or Soxhlet extraction) and the use of gas chromatography with high resolution mass spectrometry (GC-HRMS). Bioanalytical assays have also been developed for rapid screening of dioxins and DL-PCBs, including the XDS-CALUX® EPA method #4435 which has been approved as an acceptable screening method for minerals.

Toxic Equivalencies (TEQ) are used to express concentrations of dioxins (seven PCDD congeners, ten PCDF congeners) and 12 DL-PCBs in livestock feed ingredients. This is an international standardized reporting method established by the WHO. WHO-TEQs (ng WHO-TEQ/kg) are calculated by multiplying the concentration (ng/kg) of each PCDD, PCDF and DL-PCB congener by the respective WHO 2005 Toxic Equivalency Factor (TEF) (Table 1), then the values for each congener are summed to give the total WHO-TEQ. WHO-TEQs express the toxicity of each PCDD, PCDF and DL-PCB congener relative to the most toxic congener, 2,3,7,8-TCDD (van den Berg et al. 2006). Total PCB concentrations are expressed in mg/kg and are based on the sum of the concentration of approximately 72 out of 209 PCB congeners.

Table 1: The World Health Organization (WHO) 2005 Toxic Equivalency Factors (TEFs) for Dioxins, Furans and Dioxin-like PCBs

Polychlorinated Dibenzo-para-dioxins (PCDDs)
Congener TEF value
2,3,7,8-TCDD 1
1,2,3,7,8-PeCDD 1
1,2,3,4,7,8-HxCDD 0.1
1,2,3,6,7,8-HxCDD 0.1
1,2,3,7,8,9-HxCDD 0.1
1,2,3,4,6,7,8-HpCDD 0.01
OCDD 0.0003
Polychlorinated Dibenzofurans (PCDFs)
Congener TEF value
2,3,7,8-TCDF 0.1
1,2,3,7,8-PeCDF 0.03
2,3,4,7,8-PeCDF 0.3
1,2,3,4,7,8-HxCDF 0.1
1,2,3,6,7,8-HxCDF 0.1
1,2,3,7,8,9-HxCDF 0.1
2,3,4,6,7,8-HxCDF 0.1
1,2,3,4,6,7,8-HpCDF 0.01
1,2,3,4,7,8,9-HpCDF 0.01
OCDF 0.0003
Dioxin-Like PCBs (DL-PCBs) - Non-ortho PCBs
Congener TEF value
PCB 77 0.0001
PCB 81 0.0003
PCB 126 0.1
PCB 169 0.03
Dioxin-Like PCBs (DL-PCBs) - Mono-ortho PCBs
Congener TEF value
PCB 105 0.00003
PCB 114 0.00003
PCB 118 0.00003
PCB 123 0.00003
PCB 156 0.00003
PCB 157 0.00003
PCB 167 0.00003
PCB 189 0.00003

The maximum levels in livestock feed ingredients are established to limit accumulation of dioxins and PCBs in foods of animal origin, and therefore reducing human exposure. The goal is to continually reduce sources of dioxins and PCBs as much as feasibly possible to protect Canadians from unnecessary exposure to these toxic and persistent compounds. Continued feed monitoring will allow the CFIA to identify, control and eliminate, where possible, sources of these contaminants in the food chain. This approach is consistent with the Codex Alimentarius Commission's Code of Practice for the Prevention and Reduction of Dioxin and Dioxin-like PCB Contamination in Foods and Feed (CAC 2006) and the approaches taken by other regulatory agencies including the European Commission and the U.S. Food and Drug Administration.

Based on feed monitoring data collected by the CFIA from 2007-2016 under the National Feed Inspection Program, maximum levels have been established for dioxins and DL-PCBs in individual livestock feed ingredients, including: fish meal; fish oil; single mineral feed ingredients, mineral complexes/chelates/proteinates and trace mineral micropremixes; anti-caking agents; and vegetable oils and by-products of vegetable oil manufacturing. A maximum level for dioxins (seven dioxin congeners and ten furan congeners) has also been set for vegetable oils and by-products of vegetable oil manufacturing. Based on monitoring data collected from 2000 to 2006, the CFIA established a maximum level for total PCBs in marine oils approved for use as livestock feed ingredients.

All maximum levels for dioxins and DL-PCBs are expressed using the WHO-TEQ terminology, while the total PCB maximum level is expressed in mg/kg. The maximum levels for dioxins and DL-PCBs were calculated by adding two standard deviations to the mean concentration in samples of each ingredient type. The resulting values were then rounded to the nearest 0.5 ng WHO-TEQ/kg. The maximum total PCB level in marine oils was calculated by adding one standard deviation to the mean and rounding the resulting value to the nearest 0.1 mg/kg. The CFIA adopted the European Union (European Commission 2012) maximum levels for dioxins and DL-PCBs in vegetable oils and by-products of vegetable oil manufacturing directly.

Metal and Mineral Contaminants

Arsenic

Arsenic (As) is a metalloid and can be found in both inorganic and organic forms with one of four valances: -3; 0; +3; +5. Chemical and toxicological properties vary greatly depending on oxidative state and form. There are no major deposits of arsenic, rather it is found as part of other mineral ores such as copper, lead, nickel, zinc, gold, and silver. Arsenic may be released by natural or anthropogenic sources. It is released into the air through volcanic emissions, smelting, burning of fossil fuels, and application of agriculture pesticides. It is released into water through industrial effluents, weathering of rock, dissolution of salts, and atmospheric deposition (EFSA, 2005; Health Canada, 2006).

Canadian environmental releases have decreased with the raise of public concern and implementation of more stringent environmental regulations. The Canadian Environmental Protection Act included arsenic to its Schedule 1 - List of Toxic Substances in 1999. It is no longer produced commercially in Canada, and regulations limiting the use of chromated copper arsenate (CCA) pressure treated lumber were implemented in 2003 (Miningfacts.org, 2012). Arsenic based pesticides were once the dominant pesticide available but have, for the most part, been phased out. They are permitted to be used in only specific circumstances (CAREX, 2016). Apart from wood preservatives, arsenic alternatives have replaced arsenic in most products and global use has declined (IARC, 2012; Miningfacts.org, 2012).

Currently, Canada releases arsenic from base metal smelting, fossil fuel combustion, steel manufacturing, wood preservatives, and contaminated sites. The Giant Mine, a gold mine which operated from 1948 to 2004 near Yellowknife in the Northwest Territories, is of particular Canadian relevance. It contains 237,000 tonnes of arsenic trioxide waste which leaches into the nearby water sources (Indigenous and Northern Affairs Canada, 2017; Miningfacts.org, 2012). Remediation of this site is unlikely to commence prior to 2020 (Kyle, 2016).

Most Canadians are exposed to arsenic through contaminated water and food. High arsenic levels in groundwater has been identified throughout Canada, with particularly high levels being measured in certain aquifers in Alberta and Saskatchewan (Health Canada, 2006). Vegetation can accumulate arsenic from contaminated soils, water, and areal deposition, but concentrations accumulated are generally low. Aquatic organisms accumulate arsenic to a greater degree (EFSA, 2005).

The analytical methods used to detect arsenic in livestock feed and feed ingredients are electrothermal atomic absorption spectroscopy (ETAAS), inductively coupled optical emission spectroscopy (ICP-OES), and inductively coupled mass spectroscopy (ICP-MS).

Impact on Animal and Human Health

Absorption of arsenic is generally high, but depends heavily on which form of arsenic is consumed. Metallic arsenic and insoluble arsenic salts are not well absorbed. Aqueous inorganic arsenic and organic arsenic are well absorbed with estimates varying from greater than 40% to 90% absorbed in the gastrointestinal tract (EFSA, 2005; Health Canada, 2006). Arsenic is distributed through the body by binding to hemoglobin (Health Canada, 2006). Distribution to organs depends on the length of exposure. Six hours after being dosed dimethylarsinic acid, an organic metabolite of arsenic, is distributed in the following organs: kidneys, lungs, intestinal mucosa, stomach, and testes. During chronic exposure arsenic distributes to hair, skin, liver, kidneys, lung, and intestinal mucosa. In both cases, organs are listed from greatest concentration of arsenic to lowest (EFSA, 2005).

Biotransformation of arsenic species in the liver occurs rapidly. Because of the rapid metabolism, toxicity of each metabolite is not fully understood. The liver converts inorganic arsenic species to organic arsenic species. The following is one metabolic pathway proposed:

Arsenate [As5+]Arsenite [As3+]monomethylarsonous acid (MMAIII) [CH5AsO2]
monomethylarsonic acid (MMAV)[CH5AsO3]
dimethylarsinous acid (DMAIII)[C2H7AsO]
→ dimethylarsinic acid (DMAV)[C2H7AsO2]

Other pathways have also been suggested. It is probable that multiple routes of metabolism occurs at once and that there are species differences when it comes to rates and efficiency of arsenic metabolism (EFSA, 2005; IARC, 2012).

Organic arsenical veterinary drugs have been fed to poultry and swine as previous studies indicated positive effects on growth rate. New studies have demonstrated an increase of inorganic arsenic in edible tissues when these pharmaceuticals are fed. This indicates that organic arsenic biotransforms to the more toxic inorganic arsenic in vivo. As a result, in 2014, a voluntary phase out of organic arsenical based pharmaceuticals commenced in both Canada and the USA. (FDA, 2015)

Arsenic is efficiently excreted. At least half of absorbed arsenic is excreted via the urine and the rest is eliminated in bile. Exact rates and routes of excretion vary by species and individuals. Biological half-life depends on chemical form; organic arsenic has a half-life of less than 40 hours and inorganic arsenic is between 2 and 40 days. Inorganic arsenic has two rates of elimination. It is initially excreted quickly but slows down as metabolism occurs. Arsenic does not accumulate significantly in tissues (EFSA, 2010; EFSA, 2005; Health Canada, 2006; IARC, 2012).

A relative order of toxicity of different arsenic species has been established by Petrick et al. through work on human hepatocytes. From most toxic to least: MMAIII > As3+ > As5+ > MMAV = DMAV (Petrick et al., 2000). Elemental and all inorganic species of arsenic are classified as a group 1 carcinogen (carcinogenic to humans) by the International Agency for Research on Cancer (IARC). There is insufficient evidence to classify organic arsenic as carcinogenic (IARC, 2012). Generally, organic arsenic compounds are significantly less toxic than inorganic arsenic compounds with signs of toxicosis only occurring at high concentrations. Trivalent arsenic interacts with thiol-containing molecules and inhibits antioxidants. Pentavalent arsenic mimics phosphates and is substituted in biomolecules which inhibits energy conversion (IARC, 2012; NRC, 2005).

The principal clinical signs of subacute and chronic arsenic toxicity in livestock species are loss of appetite, wasting, indigestion, thirst, depression, and neurological symptoms. Symptoms of chronic oral toxicity in livestock species are seldom reported, and carcinogenic effects are rarely seen. Fish have exhibited signs of toxicosis when consuming feed with concentrations of 10 mg/kg feed in the form of inorganic arsenic. Most feeds from aquatic sources contain organic forms of arsenic. In terrestrial species, toxicosis is not expected to occur at less than 30 mg As/kg total diet (EFSA, 2005; NRC, 2005). A lower maximum level for arsenic in feed has been proposed to limit human exposure to these carcinogens.

Transfer to Food of Animal Origin

Arsenic does not effectively accumulate in foods of terrestrial animal origin when fed at low concentrations. Concentrations in tissues tend to reflect recent exposure (EFSA, 2005). Muscle is expected to contain less than 10 µg As/kg wet weight. Liver and kidneys initially sequester arsenic and tend to have higher tissue concentrations than muscle, but they are still expected to be below 50 µg As/kg wet weight (MacLachlan & Bhula, 2008). Transfer rate to muscle are species specific, 0.0017 and 0.091 have been calculated for quail and cattle, respectively (EFSA, 2005; MacLachlan & Bhula, 2008). In an analysis of laying hens, turkey, geese, ducks and pigeons, transfer to eggs was consistently low with a range of 0.010 to 0.026 (Nisianakis et al., 2009).Transfer to black tailed gull eggs was estimated to be 10% (Kubota et al., 2002). Arsenic is not efficiently excreted in milk but increases proportionally with concentrations in feed (EFSA, 2005)

In Canada, approximately 64% of arsenic exposure comes from consumption of fish and shellfish (EFSA, 2005). According to analyses conducted by Health Canada in the Canadian Total Diet Study (1993-2012), fish and shellfish have arsenic concentrations 100-1000 times higher than terrestrial foods but this is generally as the organic arsenobetaine which is not of toxicological concern (EFSA, 2010).

Contaminant Standards/Maximum Levels in Livestock Feed

Since arsenic is found in feed, control measures at the feed level remain critical to reducing contamination in foods of animal origin and therefore reducing human exposure. According to feed monitoring data collected from 1999 to 2015 by the CFIA under the National Feed Inspection Program, the types of feed commonly associated with high contamination in Canada are feeds of aquatic origin and minerals, especially zinc oxide, manganous oxide, and sulfates. The European Union has similar contaminant concentrations in fish meal and fish oils, but much lower concentrations in mineral supplements (EFSA, 2005).

Based on the review of the scientific information, the standards set by other national and international jurisdictions, and sample monitoring data, the current maximum level for arsenic in feed is sufficient to mitigate the risk of arsenic toxicity to animal health and human health. Therefore, the current maximum level of arsenic in the total diet of 8 ppm should remain unchanged.

Cadmium

Cadmium (Cd) is a rare transition metal, and generally found as a solid salt with a 2+ charge (Lide, 2004). It is typically found as a trace contaminant of zinc and copper ores and in phosphate sources. Cadmium can also be produced as a by-product of metal mining. During smelting, fossil fuel combustion, and volcanic eruptions it can partition into the air as an aerosol, contaminating the air and nearby soils (European Food Safety, 2009; Shi et al., 2012).

Canada has been one of ten top world producers of cadmium during the past 20 years (U.S. Geological Survey, 2015). Certain regions have higher cadmium soil content, such as Jamaica and parts of southwestern China (Gerald C. Lalor, 1998; Liu et al., 2015). Industries which use cadmium include zinc refineries, nickel-cadmium battery producers, recycling depots, and alloys. In addition to industrial atmospheric deposition, soil cadmium can increase with the direct application of phosphate fertilizers and sewage sludge. Both of these in turn results in vegetation accumulating more cadmium (European Food Safety, 2009).

As a known deleterious element, the use of cadmium has been decreasing on a global scale. Smelters have greater sequestering technologies and cadmium batteries are being phased out of most operations (Tolcin, 2016a). Most pigments and alloys have replaced cadmium with other less toxic metals (Tolcin, 2016b).

The analytical methods used to detect cadmium in livestock feed and feed ingredients are graphite furnace atomic absorption spectrometry (GF-AAS), electrothermal atomic absorption spectroscopy (ETAAS), inductively coupled optical emission spectroscopy (ICP-OES), and inductively coupled mass spectroscopy (ICP-MS).

Impact on Animal and Human Health

Cadmium can enter the body through inhalation or oral consumption. Inhalation exposure is important for industrial workers and smokers, but account for less than 1% of the body burden for the general public (Chen, 1994). Oral absorption of cadmium is very low. In general, it is assumed that 5% of orally consumed cadmium is taken up in the gastrointestinal tract. Absorption occurs through cadmium specific transporters and divalent metal transporters (Bressler et al., 2004; Sorensen et al., 1993). Low nutritional status, particularly low concentrations of zinc, calcium, iron, and copper result in an increased absorption rate. Middle aged women of childbearing age have the potential to absorb greater than 10% of oral cadmium (CDC, 2009). Meanwhile, well-nourished individuals will absorb less.

Once absorbed, cadmium is transported to the liver where it stimulates the production of metallothionein. Metallothionein chelates with cadmium and most of the body burden is found in this chelated form. At least 50% of the body burden is distributed in the liver and kidney, where it is primarily found in the kidney cortex (UNEP, 2010). Metabolic transformation does not occur (Van Paemel et al., 2010).

Cadmium is very poorly excreted. It has a long biological half-life with estimations in the kidney ranging from 10-30 years in humans. Other organs and tissues have a shorter half-life; liver ranges from 4.7 - 9.7 years. Excretion primarily occurs in urine, although some may occur in bile. It is estimated that <0.01% of the total body burden is excreted daily (EFSA, 2004b). At lower doses, body burden can be estimated with cadmium concentrations in the urine, but this is not accurate at higher doses because urinary excretion cadmium increases with kidney dysfunction caused by the large amount of cadmium accumulation (Friberg, 1984; Nawrot et al., 2010).

Cadmium produces toxic effects on a cellular level and by disrupting mineral balance (Rani et al., 2014; UNEP, 2010). These two mechanisms lead to toxic effects on the kidneys, bones, blood cells, liver, and gastrointestinal tract with the most well predominant effects involving the kidneys and bones (ATSDR, 2012; NRC, 2005; UNEP, 2010).

On a cellular level, cadmium binds to proteins and to antioxidants (Rani et al., 2014). Toxicity occurs when cadmium overwhelms the cell's defence mechanisms and disrupts mitochondrial pathways, leading to apoptosis. This pathway is most apparent in nephrotoxicity. Cadmium selectively accumulates in the proximal tubules. The first clinical sign of cadmium toxicity is renal damage resulting in low molecular weight proteinuria (ATSDR, 2012; NRC, 2005; UNEP, 2010).

Secondly, cadmium disrupts mineral balance. It mimics essential 2+ cations such as zinc and calcium. Osteomalacia and osteoporosis are two other common effects of cadmium toxicity. Cadmium impairs vitamin D metabolism which impacts calcium absorption and secretion (ATSDR, 2012; IPCS, 1992). Additionally, cadmium acts directly on the bone causing increased bone resorption (Brzóska et al., 2011).

Cadmium is an International Agency for Research on Cancer (IARC) group 1 carcinogen, with evidence of pulmonary cancers caused by inhalation. Carcinogenicity by oral exposure is not well established (IARC, 2016).

A low maximum level for cadmium in feed has been proposed because of its ability to accumulate. Cadmium poses a threat to health after long term exposure. Horses appear to be particularly susceptible to cadmium toxicosis because they are sensitive to mineral imbalances, such as copper (Holterman et al., 1984; Kowalczyk et al., 1986). Likewise they have a particularly long lifespan compared to other livestock species.

Transfer to Foods of Animal Origin

The liver and kidneys contain about 50% of the body burden of cadmium. These are the tissues most likely to be contaminated with high concentrations of cadmium. Accumulation does not occur in the muscle, so most meat contains fairly low cadmium concentrations even when the feed is contaminated. Cadmium is poorly transferred into milk or eggs. Milk with higher protein content tend to have higher cadmium concentrations as does milk produced early in lactation. However, the concentrations in milk have been reported to be very low.

The placental barrier effectively stops the transport of cadmium to the fetus. Likewise the follicular wall prevents the transfer of cadmium into the follicles in poultry. Eggs, especially the yolks, have very low cadmium content even when poultry consume high concentrations of cadmium (Marettová et al., 2012; Sato et al., 1997; Sharma et al., 1979; Van Paemel et al., 2010).

According to analyses conducted by Health Canada in the Canadian Total Diet Study (1993-2012), Canadian foods are below the limits set by the European Union (EU, 2008) (Health Canada, 2016).

Contaminant Standards/Maximum Levels in Livestock Feed

Since cadmium is found in feed, particularly in mineral-based feed ingredients, control measures at the feed ingredient level remain critical to reducing contamination in foods of animal origin and therefore reducing human exposure. According to feed monitoring data collected from 1999 to 2015 by the CFIA under the National Feed Inspection Program, the types of feed commonly associated with contamination are copper sulfate, phosphates, and all zinc-based minerals. These findings mimic those of the European Union (EFSA, 2004a)

Based on the review of the scientific information, the standards set by other national and international jurisdictions, and sample monitoring data, the current maximum levels for cadmium in feed are sufficient to mitigate the risk of cadmium toxicity to animal health and human health. Therefore, the current maximum level of cadmium in the total diet for horses of 0.2 ppm and the current maximum level of cadmium in the total diet for all other livestock species of 0.4 ppm should remain unchanged.

Lead

Lead (Pb) is a toxic non-essential heavy metal that is ubiquitous in the environment; originating from both natural and anthropogenic sources. While lead occurs naturally in minerals and rocks, its prevalence has increased due to emissions and waste products from mining and other industrial processes. The use of lead-containing products such as lead-acid batteries, lead paint, leaded gasoline, and lead solder in food cans has also contributed to its prevalence in the environment (ATSDR 2007). Despite having phased out lead in some of these products in the past few decades, lead exposure still remains a concern for animal and human health since it is highly toxic and does not degrade in the environment.

Lead can exist in various oxidation states and in organic or inorganic forms, but in the environment it primarily occurs in the inorganic form. The inorganic forms in which lead exists affects its environmental fate, transport, bioavailability, and in turn its toxicity (NTP 2016). Inorganic lead compounds can therefore be organized according to their toxicity (from most toxic to least toxic following oral exposure): lead acetate > lead chloride > lead lactate > lead carbonate > lead sulfide > lead sulfate > lead phosphate (EFSA 2004).

The analytical methods commonly used to detect lead in livestock feed and feed ingredients include sample preparation/sample extraction (e.g., microwave digestion) and analysis by inductively coupled plasma optical emission spectrometry (ICP-OES), graphite furnace atomic absorption spectrometry (GF-AAS) or inductively coupled plasma mass spectrometry (ICP-MS).

Impact on Animal and Human Health

Humans are exposed to lead mainly via food and water, with some exposure from air, dust, and soil (EFSA 2010). Lead absorption varies considerably depending on its chemical form, as well as the age and nutritional status of the individual (ATSDR 2007). For instance, adults typically absorb between 5-15% of the lead they ingest, whereas children absorb 30-40% due to differences in physiology and metabolism (Goyer and Clarkson 1996). Moreover, individuals with diets low in iron or calcium are prone to absorb more lead (Hammad, Sexton, and Langenberg 1996; Watson et al. 1986).

Once absorbed, lead is transported in the blood and transferred to soft tissues (e.g., liver, kidneys, and brain) (NRC 2005). Similarly to other metals, lead is not metabolized by the body and its excretion is slow. Consequently, lead accumulates in soft tissues and gradually becomes incorporated into bone during normal growth and bone metabolism processes. In fact, the majority of lead that is absorbed (about 70% in children, and up to 95% in adults) is eventually stored in bones and teeth (Thornton, Rautiu, and Brush 2001).

One of the most notable impacts of lead in humans is on the development of the brain and the nervous system of younger children (WHO 2016). These impacts have been observed at blood levels below 5 µg/dL; the level once thought as being safe. Correspondingly, young children and pregnant women are among the most vulnerable to lead toxicity. In addition, the World Health Organization's (WHO) International Agency for Research on Cancer (IARC) has classified inorganic lead compounds as probable human carcinogens (Group 2A) (IARC 2006).

Lead exhibits similar health effects in livestock species than those in humans. At lower levels, lead exposure can cause cardiovascular, neurodevelopmental, and hematological problems, and at higher and/or chronic levels, lead can cause adverse renal, gastrointestinal, hepatic, and immunological effects (NRC 2005). Livestock species are primarily exposed to lead via accidental consumption or contact with lead sources such as contaminated soil, lead ammunition, lead paint on older buildings, and lead-acid batteries. This type of exposure often leads to acute toxicity. Nonetheless, animals can also be exposed to lead through contaminated water and/or feed (EFSA 2004).

Transfer to Foods of Animal Origin

Since clearance of lead is usually incomplete and slow, lead not only accumulates in soft tissues of animals (e.g., liver, kidneys, and brain) but also gradually accumulates in their bones. On the other hand, muscle tissue does not accumulate significant amounts of lead; therefore, meat consumption is not of great concern. Concentrations of lead in milk and eggs are also generally very low. However, there is concern surrounding the consumption of offal. Although most livestock species can tolerate high levels of lead, significant accumulation of lead can occur in the liver and kidneys of exposed animals.

According to the Canadian Total Diet Study conducted by Health Canada in 1992-2012, the foods of animal origin with the highest average, median, and maximum concentration of lead were offal (liver and kidneys). Nevertheless, none of the offal sampled between 1992 and 2012 had lead concentrations greater than 35 mg/kg, which corresponds to less than 10% of the maximum European Union (EU) level for offal of bovine, sheep, pig, and poultry set by the European Commission (EFSA 2006). All other foods of animal origin also did not exceed maximum EU or Codex levels for lead.

Contaminant Standards/Maximum Levels in Livestock Feed

Since lead is frequently found in feed, particularly in mineral feed additives, control measures at the feed ingredient level remain critical to reducing contamination in foods of animal origin and therefore reducing human exposure. According to feed monitoring data collected from 1999 to 2015 by the CFIA under the National Feed Inspection Program, the types of feed with the highest average concentrations in Canada are iron oxide, zinc oxide, manganous oxide, copper chloride, copper sulfate, and diatomaceous earth. All feed samples collected from 1999-2015 were found to be compliant (i.e., did not exceed the current maximum level for lead in complete feed of 8 ppm).

Based on the review of the scientific information, the standards set by other national and international jurisdictions, and sample monitoring data, the current maximum level for lead in feed is sufficient to mitigate the risk of lead toxicity to animal health and human health. Correspondingly, the current maximum level of lead in complete feed of 8 ppm should remain unchanged.

Fluorine

Fluorine (F) is a highly toxic halogen. Under normal conditions, fluorine is a pale yellow diatomic gas. However, as the most electronegative and reactive of all elements, fluorine is able to combine with almost all elements and occurs almost exclusively in its ionic form; the halide anion, fluoride (F-) (NRC 2005). Since fluorine occurs mainly as salts, inorganic fluorides are much more abundant than organic fluorides (EFSA 2004).

Natural sources of fluorine include volcanic activity, weathering and dissolution of minerals, marine aerosols, and deep well water from areas geologically rich in fluorine (ATSDR 2003). Fluorine can also be released during aluminium and phosphate processing, as well as steel, brick, and glass production (Cronin et al. 2000). These fluorine-rich emissions can contaminate surrounding surface water, soil, and plants. In addition to natural and anthropogenic emissions, livestock feed can be contaminated by fluorine through the application of phosphate and super-phosphate fertilizers, which contain significant quantities of fluorine derived from the phosphate rocks used in their manufacturing, as well as through the addition of fluorine-bearing mineral supplements in livestock diets (e.g., high fluorine rock phosphate) (Hedley et al. 2007).

Fluorine is considered an essential element (NRC 2005), or at least a trace element with beneficial effects on the proper functioning of some enzymes, and tooth and bone development. In mammals, a diet low in fluorine may cause early tooth decay, growth retardation, impairment of fertility, and potentially osteoporosis (EFSA 2004). As a result, the drinking water from geographic regions with low natural fluorine levels is often supplemented with fluorine. Fluorine is also routinely added to calcium products and dental care products.

Mobility of fluorine in soil is very limited and most plant species have a limited capacity to absorb fluorine from the soil (Hedley et al. 2007). Nonetheless, approximately 75% of fluorine present in plants is absorbed by ruminants (Shupe et al. 1962), while up to 40 and 50% of fluorine contained in soil is absorbed by bovine species and sheep, respectively (Grace et al. 2003; Wöhlbier et al. 1968). Since forage normally contains only 2 to 20 mg/kg fluorine, soil ingestion during grazing may contribute to more than 50% of the dietary fluorine in sheep and cattle (Cronin et al. 2000). Fluorine compounds with low solubility (e.g., calcium, magnesium, and aluminium fluorides) are poorly absorbed compared to fluorine ions released from readily soluble fluorine compounds (e.g., sodium and hydrogen fluoride), as well as fluorosilicic acid and monofluorophosphate (EFSA 2004).Bioavailability and absorption of fluorine depends on the form, route of exposure, and solubility of the fluorine compound, as well as the species and gastrointestinal and nutritive conditions of the animal.

Once absorbed, fluorine is mainly sequestered in bones and teeth (Kaminsky et al. 1990). In fact, approximately 99% of body burden of fluorine is associated with these tissues (NRC 1980). Only minor concentrations of fluorine are measurable in body fluid and soft tissues (Grace et al. 2003). However, fluorine has been shown to transfer through the placental barrier to the developing fetus in rats and humans (Gedalia et al. 1961; Theuer et al. 1971). Fluorine is rapidly eliminated from the body, mostly through urine (EFSA 2004; Grace et al. 2003). Nevertheless, only about half of ingested fluorine is actually excreted; the remainder accumulates in bones and teeth (EFSA 2004).

The analytical methods commonly used to detect fluorine in livestock feed and feed ingredients are ion-selective electrode (ISE) and ion chromatography (IC).

Impact on Animal and Human Health

Although fluorine is an essential element, at high concentrations it can impact the health of animals and humans. Excess fluorine intake can cause dental and skeletal fluorosis; although, skeletal fluorosis requires longer chronic exposure (Livesey and Payne 2011). Indeed, dental fluorosis is the earliest visible sign of chronic fluorosis in mammals. This type of fluorosis affects teeth during development and produces dental abnormalities. Skeletal fluorosis can disrupt osteogenesis, accelerate bone metabolism, produce abnormal bones (exostosis, sclerosis), and accelerate bone resorption (osteoporosis) (NRC 2005). Correspondingly, skeletal fluorosis causes stiffness and lameness in animals. Dietary exposure to fluorine can ultimately cause extreme weight loss, decreased food consumption, reduced milk production, and arrested development (Phillips and Hart 1935; Phillips et al. 1934).

The risk of fluorosis associated with livestock feed depends on the form, dose, and duration of fluorine exposure, the species of livestock, the physiological and nutritional status of the animal, and the location and grazing management of the farm (EFSA 2004; Livesey and Payne 2011). For instance, animals with low calcium diets or a calcium imbalance, as well as those who are pregnant or lactating, are more vulnerable to fluorosis. In addition, the livestock species most susceptible to fluorosis is cattle, closely followed by horses and sheep; chickens are the most tolerant (Suttle and Underwood 2010).

Contaminant Transfer to Foods of Animal Origin

Due to low transfer rates and its affinity for mineralized tissues, fluorine levels are very low in soft tissues (generally <2.5 mg/kg wet weight), even when dietary exposure is high (EFSA 2004). Only tendon, aorta, placenta, and kidney may have Qhigher fluorine concentrations (EFSA 2004; Livesey and Payne 2011). Fluorine levels in cow's milk are normally very low, except when fluorosis occurs in cattle (NRC 2005). Similarly, accumulation of fluorine in eggs, which mostly occurs in the yolk, only arises when birds are fed high-fluorine diets (Phillips et al. 1935). Therefore, the risk of transfer of fluorine to humans from the consumption of foods of animal origin is low. In addition, fluorine consumed from water and beverages accounts for more than 70% of total fluorine intake in humans (NRC 2005). However, regular consumption of marine fish and crustaceans can significantly increase fluorine intake. This is because high fluorine concentrations may be found in the tissues of these aquatic species (up to 26 mg F/kg wet weight) (Camargo 2003).

Contaminant Standards/Maximum Levels in Livestock Feed

Although the transfer of fluorine to foods of animal origin is low, elevated levels of fluorine have been reported in crops contaminated by fluorine-bearing dusts, fumes, pesticides, and water, as well as in mineral feeds such as rock phosphates, and in marine-based feed ingredients and bone meals (Moren et al. 2007). Consequently, control measures at the feed ingredient level remain critical in reducing contamination in foods of animal origin and human exposure.

Based on the review of the scientific information and the standards set by other national and international jurisdictions, the current action levels for fluorine in feed is sufficient to mitigate the risk of fluorine toxicity to animal and human health. Correspondingly, the current maximum levels of fluorine in complete feeds and mineral feeds in Section 19(1)(b) of the Feeds Regulations should remain unchanged and amount of 150 mg/kg should be included for feeds for other livestock species.

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