The ZRT Laboratory Blog

ZRT Dried Blood Spot COVID-19 IgG Antibody Testing: An Update

Tue, 11 May 2021 12:19:59 -0700

When the COVID-19 pandemic began to threaten the United States in early 2020, ZRT began work on dried blood spot (DBS) COVID-19 antibody testing. This was prior to the molecular (polymerase chain reaction or PCR) testing boom starting in mid-2020 that eventually became the most dominate and useful test for detecting current COVID-19 cases using nasal/oral samples. Antibody testing took a backseat to molecular testing for most of 2020, but with rapidly dropping case counts and the introduction of vaccines, antibody testing is making a comeback for research, public health surveillance, and clinical testing in 2021.

ZRT’s IRB-Approved COVID-19 Study

ZRT Laboratory received Institutional Review Board (IRB) approval to collect health care provider assisted matching serum and finger stick DBS samples in mid-2020. A total of 177 matching samples were used to validate the ZRT DBS COVID-19 IgG S1 Spike and Nucleocapsid Antibody Tests, which is detailed in our December 2020 scientific publication, “Validation of dried blood spot sample modifications to two commercially available COVID-19 IgG antibody immunoassays” (Bioanalysis, 2021). Amendments to ZRT Laboratory’s study allowed us to look at a vaccine-induced immune response, which will be the focus of a second manuscript to be peer-reviewed for publication.

New Nucleocapsid Antibody Test Update

ZRT recently updated the DBS COVID-19 IgG Nucleocapsid Antibody Test in early 2021 from the one detailed in our publication to improve test performance and simplify methodology. The combination ZRT DBS COVID-19 IgG S1 Spike and Nucleocapsid Dual Antibody Test is available for research and public health surveilance only. Positive and negative concordance between serum and DBS showed excellent agreement at 100%/99.3% and 100%/100% for the S1 spike and nucleocapsid assays respectively.

How is COVID-19 Antibody Testing Useful?

COVID-19 IgG antibody testing is increasing in popularity because the majority of vaccines, including the Moderna, Pfizer-BioNTech, Johnson & Johnson, and AstraZeneca produce an anti-SARS-CoV-2 spike immune response that is only detectable using COVID-19 antibody tests that look for antibodies against the SARS-CoV-2 spike protein.

Research and public health surveillance interest for the ZRT DBS COVID-19 IgG S1 Spike and Nucleocapsid Dual Antibody Test has increased significantly as the S1 spike can detect a vaccine immune response while the nucleocapsid assay will only detect a past native COVID-19 infection. This is important for seroprevalence studies to track increases in native COVID-19 infections in a population as vaccines are rolled out.

Below is an example of spike and nucleocapsid antibody levels detected over time post vaccination in an individual with no past native COVID-19 infection. Spike antibody titers (levels) increase while nucleocapsid titers show no increase. A past native COVID-19 infection would likely show and increase in both spike and nucleocapsid antibody titers.

Native Infection vs Vaccine Immune Response: Real-World Example

Recent research at ZRT has shown real-world examples of a population actively being vaccinated and the ability to detect native COVID-19 infections in this group.

Below is an example where study participants may or may not have received a COVID-19 vaccine. Possible native COVID-19 infections have been highlighted with red arrows on the matching spike and nucleocapsid antibody tests since vaccines do not produce an immune response against the SARS-CoV-2 nucleocapsid protein.

The Future of COVID-19 Antibody Testing

ZRT Laboratory expects COVID-19 antibody testing to outpace molecular (PCR) testing in the future. As vaccinations continue, the amount of protection against a COVID-19 infection may be related to vaccine antibody titers, which diminish over time like a native COVID-19 infection. How this impacts future risk for infection with SARS-CoV2 variants is unknown. So far, vaccines that produce the highest antibody titers (Moderna and Pfizer-BioNTech) have shown the highest efficacy in phase III trials. Moving antibody testing from qualitative (negative, indeterminate, positive) to semi-quantitative (negative, indeterminate, low-positive, mid-positive, high-positive) or quantitative (true antibody titer amount) could help indicate when booster vaccines should be considered, as each individual has a varying immune response to vaccines.

“Long COVID”

The term “long COVID” has been given to people with a past COVID-19 infection who continue to experience symptoms months from infection. This can include people with asymptomatic COVID-19 infections who only express symptoms after the immune system has eliminated the virus. As we learn more about long-term adverse symptoms and conditions associated with COVID-19, referred to as “long COVID,” the suite of endocrine testing offered by ZRT Laboratory will help shed light on why some individuals have very slow recovery from COVID-19. Biomarkers such as sex-steroid hormones, cortisol, thyroid hormones, insulin, inflammatory cytokines, etc., that are closely associated with SARS-CoV-2 infections and problems with recovery (long Covid) are tested in finger-prick dried blood spots, dried urine, and saliva samples that can easily be collected at home and sent to ZRT Laboratory for testing.

It is not clear when the COVID-19 pandemic will end, but it is clear that clinical and research laboratory testing will continue to be a key tool in understanding individual differences in recovery from COVID-19 and how this relates to vaccines, and any future viral variants that may arise.

COVID-19 At-Home Sample Collection – FDA Does Not Approve (Yet)

Wed, 25 Mar 2020 09:18:39 -0700

If there is anything the United States is lacking in the war against the 2019 novel coronavirus (SARS-CoV-2) is the mass testing required to detect the virus in those with suspected cases and in asymptomatic individuals. In February the Department of Health and Human Services declared a public health emergency, which allowed for “emergency use of in vitro diagnostics for detection and/or diagnosis of the novel coronavirus (2019-nCoV).” The goal was to speed up new test development and commercialization to increase testing capability in the United States. It wasn’t clear what laboratories had the green light to commercialize a COVID-19 test and whether they would need FDA review and approval before release.

The Rush to Develop COVID-19 Testing

Many private, public, and reference laboratories rushed to develop, validate and commercialize testing after learning of the U.S. Food and Drug Administration (FDA)’s emergency guidance. This process normally takes months or years, but the FDA’s emergency use of diagnostics allowed for expedited validations and commercialization. Laboratories are focusing on RT-PCR technology (reverse transcription polymerase chain reaction), which is used and recommended by the Centers for Disease Control and Prevention (CDC), and serology testing, which looks at antibodies produced in response to infection using serum, plasma or whole blood. The RT-PCR test shows current infections while the serology testing is only useful for result confirmation or confirming exposure post-infection.

At-Home vs At-Home Collection vs Standard Laboratory vs Point-Of-Care Testing

At-Home Testing – A device that is FDA approved and purchased over the counter without doctor approval. Sample is collected at home and applied to the testing device. Results take minutes and are qualitative. The FDA will likely never approve these for COVID-19 testing as they don’t want people self-diagnosing or misinterpreting results. An example is a home pregnancy test. Be aware of fraudulent devices and claims. You can check the FDA registry for approved devices here.

At-Home Collection – After doctor approval, a collection kit and return shipping material is sent to the patient for sample collection at home. The sample is mailed back to a laboratory for analysis. Results take >3 days from time of collection. Example: https://www.zrtlab.com/sample-types/dried-urine/.

Standard Laboratory Testing – A medical professional collects a sample and sends it to a laboratory for testing. Results typically take >1 day from time of collection. Example: https://www.labcorp.com/tests/139900/2019-novel-coronavirus-covid-19-naa.

Point-Of-Care Testing – An FDA approved test that can be run in a doctor’s office or hospital with minimal training. Results can be available in minutes. Example: https://www.cepheid.com/coronavirus.

Laboratories that develop and commercialize at-home collections for testing, otherwise called laboratory developed tests (LDTs), are considered high-complexity laboratories that require CLIA (Clinical Laboratory Improvement Amendments) certification to operate. CLIA is overseen by the FDA, Center for Medicaid Services (CMS), and the Centers for Disease Control (CDC). The FDA has a final say on what LDTs can be brought to market and can force a laboratory to cease operation if they believe testing is fraudulent or misleading. The most difficult approval is for FDA point-of-care testing because the test manufacturer must show that someone with limited knowledge of the test can produce accurate results on a fool-proof system. ZRT Laboratory is an example of a high-complexity laboratory with CLIA certification that offers home collection options for saliva, finger-stick dried blood spots, and dried urine that are sent to ZRT and assayed by LDTs developed under FDA/CLIA guidelines.

Current Problems with At-Home Collection COVID-19 Testing

At the moment there are a couple of problems with at-home collection COVID-19 testing.

Nasopharyngeal/oropharyngeal swabs used for the RT-PCR test require them to be deeply inserted as shown here. This is very uncomfortable and should only be attempted by a medical professional. The sample may not be properly collected if not inserted deeply enough or long enough. This should not be attempted by an individual at home.
Testing supplies are in high demand right now, and all resources should be directed toward hospitals and screening centers that are running low on supplies.
A patient showing COVID-19 symptoms will be the one removing kit contents, taking the test, placing specimens in a shipping container or pack, and mailing everything back to the laboratory. This potentially exposes mail carriers to the virus. There are strict guidelines for shipping COVID-19 specimens that the average person may not understand.
Laboratory developed tests rely on self-validation to prove they are accurate and reliable. There may be false negative results that go undetected and influence personal/medical decisions. This is very difficult to control if laboratories aren’t running standardized CDC/FDA approved testing. Rapid test development and validation only increases the chances of inaccurate results and hidden assay problems.
Testing for profit. Unfortunately, many laboratories will be looking to profit from panic. Those claiming to run testing “at-cost” should break down the costs of all parts of testing including kit supplies, shipping, assay prices, and laboratory operation.

FDA Halts At-Home Testing for COVID-19

The FDA recently halted all at-home collections for COVID-19 testing. Without FDA approval, which likely will take months for current laboratory developed tests, do not expect at-home collection for COVID-19 testing until at least May/June. A new type of collection (saliva, nasal swab, dried blood spot, feces) will need to be validated and approved to replace nasopharyngeal/oropharyngeal swabs and conventional blood draws. ZRT Laboratory is investigating the possibility of using dried blood spots in concert with serology antibody testing for COVID-19, but we will need to continuously monitor the FDA’s position on at-home collections before moving forward with test development, validation, and commercialization.

Preventing and Protecting Against COVID-19 – Is Selenium the Answer?

Tue, 25 Feb 2020 13:31:24 -0800

It seems like there is an endless loop of stories these days about new viruses and the spread of disease. There is no doubt that as the human population increases and the space between us decreases, we will only experience more of these events in the future. While the world waits on new vaccines, one solution to slowing or preventing the spread of viruses may be something as simple as adequate selenium nutrition.

How Selenium Protects Against Viral Infections and Mutations

Adequate selenium nutrition should be considered as a defense against viral infectious diseases.

Selenium is an essential micronutrient that is important for immune response, thyroid health, oxidative damage prevention, and many other functions. Selenium from our diet replaces a sulfur atom in the amino acid cysteine to form selenocysteine, which is then incorporated into selenoproteins. There are 25 known selenoproteins, with most of them exhibiting antioxidant properties such as glutathione peroxidase (GPx). Viruses produce reactive oxygen species (ROS) which are combated by GPx and other selenoproteins to slow down viral replication and mutations [1,2]. Studies using mice have shown that viral symptoms and infection times are more severe when dietary selenium is deficient, and that low selenium intake results in decreased GPx activity [3,4]. While selenium may not be the only nutrient that slows or prevents viral damage and mutation, adequate selenium nutrition should be considered as a defense against viral infectious diseases.

In a nutshell, selenium deficiency → increased viral oxidative stress/inflammation → increased viral damage and mutations → new viral strains.

Selenium Deficient Soil and Connection to New Viruses

A publication from 2011 [5] links the evolution and spread of viral infectious diseases (HIV/AIDS, influenzas, SARS, Ebola, Swine Flu, Bird Flu) to areas where soil selenium levels are lower. A map in the article overlays areas of soil selenium deficiency with the origin of new viruses. Countries like China, where selenium-deficient soil is widespread and city populations number in the millions, are most susceptible to viral evolution and spread.

Selenium Deficiency and Heavy Metals

Excessive arsenic and mercury exposure can deplete selenium because of their high affinity for each other, leaving little selenium left to perform all its essential functions. In areas with elevated environmental and/or industrial levels of heavy metals, selenium sufficiency becomes even more important. Arsenic from well water and mercury from coal fired power plants and seafood are some of the greatest dangers.

How Can We Ensure Selenium Adequacy?

ZRT Laboratory has a blood spot and dried urine test for selenium and other essential and heavy metals run by inductively coupled plasma mass spectrometry (ICP-MS), the gold standard in element analysis. Blood tells a different story than urine, which is why we recommend testing both sample types for selenium. Elements such as zinc, copper and iodine are also involved in immune system health and should be monitored simultaneously. ZRT has been involved in research projects spanning the globe because of the collection and shipping ease of dried sample collections, and we have seen first-hand where selenium deficiency is a serious problem. Luckily in the United States we have many foods fortified with selenium, and selenium sufficient soil in the heartland where grains are primarily grown. While selenium supplementation is an effective way to increase selenium intake, too much selenium can also be dangerous. Learn more about selenium sources, daily intake, and selenium deficiency/excess.

Related Resources

References

[1] Sanjuán R, Domingo-Calap P. Mechanisms of viral mutation. Cell. Mol. Life Sci. 2016;73:4433–4448.

[2] Guillin OM, et al. Selenium, Selenoproteins and Viral Infection. Nutrients. 2019;11:2101.

[3] Beck MA, et al. Selenium deficiency increases the pathology of an influenza virus infection. FASEB J 2001;15:1481-3.

[4] Beck MA, et al. Benign human enterovirus becomes virulent in selenium-deficient mice. J Med Virol. 1994;43:166-70.

[5] Harthill M. Review: Micronutrient Selenium Deficiency Influences Evolution of Some Viral Infectious Diseases. Biol Trace Elem Res 2011;143:1325–1336.

ZRT’s Laboratory Developed Tests - How We Bring Innovative Dried Sample Testing to Market

Fri, 27 Dec 2019 11:51:20 -0800

ZRT Laboratory has been working with dried samples for over 15 years, and the number of tests we offer using dried urine and blood spot make us the world expert on dried sample validation and commercialization. ZRT Laboratory specializes in dried sample types because of their superior stability, ease of collection, simple shipment and reduced storage space. Dried urine and blood spot collection is popular with researchers and remote clients, as these sample types open the door for testing in locations that lack refrigeration and equipment necessary for liquid sample collection.

In order to offer clinical testing using dried samples, ZRT Laboratory must go through a rigorous validation process for each analyte. If validation is successful and the test is commercialized, it is considered a Laboratory Developed Test (LDT). LDTs are overseen by the Centers for Medicare and Medicaid (CMS)/Clinical Laboratory Improvement Amendments (CLIA) and the Food and Drug Administration (FDA), and can only be performed at the laboratory completing the validation.

The following is a real example of the test validation process for an LDT – in this case the dried urine rare elements assay (gadolinium [Gd], thallium [Tl], uranium [U], and creatinine) run by Inductively Coupled Plasma Mass Spectrometry (ICP-MS).

Clinical Usefulness

The first thing considered before a test is developed and validated is its clinical usefulness. It is important to choose the appropriate sample type and be able to explain results. This is usually a multi-week process of researching scientific literature while determining routes of excretion and expected concentrations.

Method Development

The method development process can be simple or complex depending on whether there is an established liquid method as a starting point. Multiple filter paper lots need to be screened to check for consistency, and extraction efficiency needs to be tested. Some methods require a concentrated sample for maximum sensitivity while others need further sample dilution, so sample requirements and extraction volume must be determined. The dried urine rare elements assay, for example, must be able to test down in the low parts-per-trillion (ppt), so a concentrated sample is needed.

Preparing (Drying) Samples

All samples used during the validation process, which include standards, calibrators, controls, spikes, patient samples, blanks, and proficiency samples, are dried on laboratory grade filter paper and stored in a -20°C freezer. Some samples are left at room temperature and others refrigerated or heated for stability testing under different storage conditions, which is a part of the validation.

Accuracy

Accuracy testing is the most important part of the validation process. This covers extraction efficiency of sample from filter paper and verifies that standards and calibrators are performing properly. Accuracy also ensures that results obtained at different laboratories are comparable. For this purpose, external proficiency samples are tested, if available. In the case of the rare elements assay, thallium proficiency samples are available through the College of American Pathologists Trace Metals Urine Program (CAP-TMU). Liquid proficiency samples are dried on filter paper, run as a “patient sample,” and compared to expected values when results are available. Split samples are also sent to reference laboratories for comparison.

Inter-Assay and Intra-Assay Precision

Inter- and intra-assay precision looks at the amount of variation between identical samples run on a single day and over a month period (10+ replicates of each). The coefficient of variation (%CV = Standard Deviation/Average X 100) is used to judge assay variation, with <20% considered acceptable. Inter-assay precision includes samples kept at room temperature, refrigerated and frozen to test for stability under all conditions. Heated samples at 38°C (100°F) are also tested in a week-long study to replicate samples being left in a hot area such as a mail van.

Limit of Blank, Detection and Quantification

The limit of blank (LOB), limit of detection (LOD), and limit of quantification (LOQ) help determine the smallest amount of analyte that can reliably be detected. Twenty blank and low concentration samples are used to determine LOB and LOD, while LOQ is based on other parts of validation like linearity. In most cases LOD and LOQ are identical, but this must be confirmed.

Linearity and Spike Recovery

Linearity testing involves diluting samples using extracted blank to make sure the low, mid, and high ranges of the assay are acceptable. Linearity also confirms that the assay is linear down to the LOD. Spike recovery is performed to show that when a known amount of analyte is added to a sample, the assay result increases by that set amount.

Interference

Interference can be tested in different ways. For hormone assays you may look at interferences from hormones with a similar structure, but for ICP-MS a potentially interfering element is spiked into a sample, then blank is spiked into a second identical sample, and results run and compared. The following is an example of barium interference on gadolinium and what an interference-free run looks like for thallium.

Explanation: Gadolinium155[14.8% abundance] has a known interference from Barium Oxide at mass 155 (Barium138[71% abundance]+Oxygen17[0.038% abundance]). The concentration of barium tested was 1 mg/L. The geometric mean barium level measured in the U.S. general population aged 6 and older is reported by the CDC as 1.56 µg/g creatinine. This level is >600x higher than that used in the spike solution. Barium is therefore not expected to be a problem in gadolinium analysis.

Reference Range

Each laboratory must develop their own analyte reference range that ideally represents a healthy testing population. At ZRT Laboratory we de-identify patient samples from prior testing or set up a collection study to obtain samples, and typically run 500+ samples to establish ranges. Generally, a 5th-95th percentile is used, but it is dependent on the analyte and literature. A 5th-95th percentile means that ideally 5% of people testing will be low and 5% will be high. This is meant to detect outliers, not necessarily deficiency or toxicity. The rare elements gadolinium, thallium, and uranium are non-essential elements, so the reference range is set at >95%, which includes creatinine correction to adjust for hydration of the test subject.

Wrapping up Validation

There are many other small tests that are necessary to complete validation. These include lab technician comparisons, filter paper lot variation and background interference, creatinine correction studies, sources of contamination and an acidified filter paper comparison (since acidified filter paper is used for some ZRT testing). The entire process may take as little as 3 months to as long as years and may need to be restarted from scratch if a step fails.

Future Developments

We continue to expand our dried sample test offerings with ongoing plans to add new sample types. You can check out the current list of dried sample tests we offer on our sample types page. If you are interested in testing that ZRT Laboratory doesn’t currently offer, you can visit our research collaboration page to propose a dried sample test that fits your needs.

Related Resources

Pacific Northwest Wild Mushrooms – Nutrients from the Forest Floor

Fri, 04 Oct 2019 16:34:43 -0700

Here in the Pacific Northwest we have a large variety of choice wild edible mushrooms. Many of these mushrooms cannot be cultivated, making them rare delicacies that are only found if the soil, weather, elevation, trees, temperature, etc. are just right. After the rains fall, I head to the forests in search of delicious and nutritious edible fungi.

Mushroom hunting is a hobby shared by many, but what some foragers may not know is they are a great source of nutrients and vitamins. Here are some of my favorite mushrooms to hunt for and the unique benefits of each.

*Warning* - Wild mushrooms need to be properly identified before consumption. It is best to consult a professional to confirm finds are not poisonous, and “when in doubt, throw it out”.

Morels (Morchella sp.)

Summer fires have become more common in the Pacific Northwest, but with them come morels in spring. Morels are typically associated with pine trees growing at elevations >3000 ft where snow is abundant during the winter. The combination of nutrients from a wildfire mixed with the moisture from rapidly melting snow results in a phenomenon that has people flocking to charred landscapes in April/May. This mysterious mushroom has one of the highest vitamin D contents of any wild mushroom, at 206 IU/100 g fresh weight [1]. Morel mushrooms contain powerful antioxidants which prevent cellular damage caused by reactive oxygen species (ROS); but more research is needed to identify the specific compounds responsible [2]. Amino acids (glutamic acid, alanine), fatty acids (linoleic, oleic, palmitic), and organic acids (oxalic, quinic, malic, citric) are also present at high levels [3].

Golden Chanterelle (Cantharellus formosus)

Chanterelles are the state mushroom of Oregon. They are easy to identify, are plentiful in dark and damp old growth forests, and are packed full of nutrients. When heavy rains begin in the fall, expect to see the gold color popping up from beneath forest litter. Chanterelles are high in potassium and B-vitamins, and like morels, have one of the highest natural concentrations of vitamin D [4,5]. The golden chanterelle grows slowly for over a month, so it needs a natural insecticide to prevent its destruction before releasing spores. It is believed that by having high levels of vitamin D, only 1% of chanterelles are damaged by insects while other mushrooms containing only trace levels of vitamin D are 40-80% insect invaded [6].

Lobster Mushroom (Hypomyces lactifluorum)

Lobster mushrooms are bizarre. They are a parasitic fungus that attacks a mushroom (typically Russula or Lactarius), completely changing the color, smell, interior, exterior, and potential toxic properties. A lobster mushroom has the color of a lobster and a mild seafood smell/flavor. For this reason, they are used as a seafood substitute/addition in soups and other dishes. I typically find them when looking for chanterelles. They are an excellent source of vitamin D and their nutrition seems to vary depending on the host mushroom. It is rumored that people sensitive to iodine and shellfish can react to lobster mushrooms, indicating that high levels of iodine or a protein common in seafood may be present (at least it smells like it!)

Porcini/King Bolete (Boletus edulis)

The porcini mushroom can be found in many different environments, from sandy soils near the beach to dense dark forests high in the mountains. I commonly find them in the springtime when looking for morels or during summer months while hiking through coastal shore pines. They are prized for their flavor and aroma. Porcini have a very high level of selenium compared to other popular edible mushrooms [7]. They are also high in fiber, proteins, amino acids, antioxidants (ergothioneine and glutathione), and the elements potassium, calcium, magnesium and zinc [8,9].

Oregon White Truffle (Tuber oregonense)

One of the rarest wild mushrooms is the Oregon white truffle. It is commonly associated with medium growth fir trees and hides under a layer of duff, making it very difficult to find without the help of hungry squirrels or truffle dogs. Truffles are prized for their potent aroma used to enhance dishes, and they are believed to be an aphrodisiac. Truffles provide nutrients to the tree and the tree provides sugar in return though a complex mycorrhizae network. Truffles are high in fat, protein, essential amino acids, and the essential elements iron, copper, zinc and manganese [10].

Lion’s Mane (Hericium erinaceus)

Lion’s mane is an unmistakable mushroom. It is often large, white, and looks like a lion’s mane. I have only found a couple of them in nature, but the size itself provides plenty to eat. It is found on decaying hardwood like oak, birch and walnut in the spring and fall. Lion’s mane is well known for its health benefits, specifically relating to the nervous system and brain. It is commonly added as a powdered ingredient to brain-boosting and superfood products. As one study outlines, lion’s mane health properties include “antibiotic, anticarcinogenic, antidiabetic, antifatigue, antihypertensive, antihyperlipidemic, antisenescence, cardioprotective, hepatoprotective, nephroprotective, and neuroprotective properties and improvement of anxiety, cognitive function, and depression.” [11] Lion’s mane contains hericenones and erinacines, compounds which stimulate nerve growth factor (NGF), a neuropeptide that helps maintain and organize neurons [12]. Some animal studies have shown an increase in BDNF after consuming lion’s mane mushrooms, but more research is needed [13,14].

The Dark Side of Mushrooms…

While mushrooms are high in nutrients, they are also known for absorbing chemicals (fertilizers, pesticides, herbicides) and heavy metals (lead, arsenic, cadmium, aluminum, and mercury). As a rule of thumb, I never pick mushrooms along trails or roads, clear-cuts, golf courses, within the city boundaries, or any other place exposed to chemicals or pollution. It’s better to be safe than sorry. If you commonly consume mushrooms (wild or cultivated) or products containing mushrooms (powders, pills, cosmetics), it is a good idea to test yourself for heavy metals and essential elements.

Foraging for wild mushrooms is as challenging as it is rewarding. Luckily in the Pacific Northwest we have opportunities year-round to search for choice edible fungus. It is pretty neat that mushrooms are the only natural source of vitamin D in the produce aisle, but you may be paying a pretty penny at the grocery store for morels, chanterelles, lobsters, and king boletes unless you get out in the forest and find some … just don’t tell anyone your spot!

Related Resources

References

[1] Phillips KM, et al. Vitamin D and sterol composition of 10 types of mushrooms from retail suppliers in the United States. J Agric Food Chem. 2011;59(14):7841-53.

[2] Nitha B, et al. Evaluation of free radical scavenging activity of morel mushroom, Morchella esculenta mycelia: a potential source of therapeutically useful antioxidants. Pharm Biol. 2010;48(4):453-60.

[3] Tietel Z, Masaphy S. True morels (Morchella)-nutritional and phytochemical composition, health benefits and flavor: A review. Crit Rev Food Sci Nutr. 2018;58(11):1888-1901.

[4] Watanabe F, et al. Characterization of vitamin B₁₂compounds in the wild edible mushrooms black trumpet (Craterellus cornucopioides) and golden chanterelle (Cantharellus cibarius). J Nutr Sci Vitaminol (Tokyo). 2012;58(6):438-41.

[5] Cardwell G, et al. A review of mushrooms as a potential source of dietary vitamin D. Nutrients. 2018;10(10).

[6] https://www.madaboutmushrooms.com/mad_about_mushrooms/2015/01/chanterelles-101-post-script.html

[7] Falandysz J. Selenium in edible mushrooms. J Environ Sci Health C Environ Carcinog Ecotoxicol Rev. 2008;26(3):256-99.

[8] Falandysz J, et al. Multivariate characterization of elements accumulated in King Bolete Boletus edulis mushroom at lowland and high mountain regions. J Environ Sci Health A Tox Hazard Subst Environ Eng. 2008;43(14):1692-9.

[9] Kalaras MD, et al. Mushrooms: A rich source of the antioxidants ergothioneine and glutathione. Food Chem. 2017;233:429-433.

[10] Patel S, et al. Potential health benefits of natural products derived from truffles: A review. Trends in Food Science & Technology. 2017;70:1–8.

[11] Friedman M. Chemistry, Nutrition, and Health-Promoting Properties of Hericium erinaceus (Lion's Mane) Mushroom Fruiting Bodies and Mycelia and Their Bioactive Compounds. J Agric Food Chem. 2015;63(32):7108-23.

[12] Lai PL, et al. Neurotrophic properties of the Lion's mane medicinal mushroom, Hericium erinaceus (Higher Basidiomycetes) from Malaysia. Int J Med Mushrooms. 2013;15(6):539-54.

[13] Chiu CH, et al. Erinacine A-Enriched Hericium erinaceus Mycelium Produces Antidepressant-Like Effects through Modulating BDNF/PI3K/Akt/GSK-3β Signaling in Mice. Int J Mol Sci. 2018;19(2). pii: E341.

[14] Park YS, et al. Effect of an exo-polysaccharide from the culture broth of Hericium erinaceus on enhancement of growth and differentiation of rat adrenal nerve cells. Cytotechnology. 2002;39(3):155-62.

Heavy Metals in the Garden: Are Your Home-Grown Fruits and Vegetables Safe for Consumption?

Thu, 13 Jun 2019 14:29:48 -0700

Growing your own fruits and vegetables is both challenging and rewarding. Many people plant gardens with the expectation that they can control what goes into their food. Gardening, especially in urban areas, has grown in popularity, but unfortunately, it comes with some risks. Contamination with elements present in the air, soil, or groundwater is a concern in both urban and rural gardens, and fruits and vegetables are good accumulators of heavy metals. This blog post details sources of heavy metal contamination and what you can do to help prevent soil contamination and heavy metal exposure from home-grown fruits and vegetables.

How Do Heavy Metals Get into My Garden?

There are many natural and anthropogenic [anthropogenic = originating from human activity] sources of heavy metals. Accumulation of these contaminants in soil typically occurs over a long period of time and may be from multiple sources. Here is a list of common sources of heavy metals.

Vehicle exhaust
Coal fired power plants
Industrial waste
Mine waste
Well/irrigation water
Fertilizers/pesticides
Paint chips
Natural events (volcanoes, floods, etc.)

Soil around areas of heavy traffic has been shown to contain higher levels of lead, which is concerning for the urban gardener.

Which Heavy Metals Are Most Concerning?

Lead – Lead is a major contaminant of soil due to its past use in gasoline, plumbing pipes, and paint. Soil around areas of heavy traffic has been shown to contain higher levels of lead, which is concerning for the urban gardener. Lead paint on the exterior of old houses can flake off or be blown into soil. Water coming from leaded pipes and fittings can also contaminate soil. The good news is that the use of lead in gasoline, pipes and paint is now banned in the US.

Cadmium – Green leafy vegetables and grains are the largest source of cadmium in non-smokers, while smokers are at greatest risk from use of tobacco which is a good cadmium accumulator. Cadmium primarily comes from fertilizers and pesticides but can also come from waste water and industrial emissions. Cadmium is readily absorbed by plants [1].

Arsenic – Arsenic is often found in well water used for irrigation. Old apple orchards used lead arsenate as a pesticide, so many old apple orchards are contaminated with both arsenic and lead.

Thallium/Mercury – Coal-fired power plants are the greatest source of anthropogenic thallium and mercury. Soil located around coal fired power plants has been shown to have higher levels of these two heavy metals.

Zinc/Copper/Manganese – Although considered essential elements, zinc, copper and manganese can be toxic at high enough concentrations. Fertilizers, mine waste, and natural sources can result in high soil concentrations of these elements.

Bioaccumulation of these heavy metals is a big contributor to their adverse health effects.

How to Reduce Heavy Metal Contamination in Soil and Produce

Here are a few ways to ensure heavy metal contamination in your garden is reduced or prevented.

A soil test for heavy metals is the best way to determine what contaminants are present.
A well water test will help identify a contaminated aquifer or naturally high amounts of heavy metals like arsenic.
It can be very difficult to remove heavy metals from soil, so using a raised planter with clean topsoil can reduce exposure.
Plant gardens away from traffic and old buildings. Trees are good barriers that can block wind-blown dust and air pollution [2]. Increased soil contamination has been linked to closer proximity to roads [3].
Keep soil at a neutral pH of 6.5-7. Lead is not readily absorbed by plants unless the soil is very acidic [4]. Use soil amendments to raise the pH if necessary.
Plant fruits and vegetables that arise from flowers, as heavy metals tend to accumulate in root, leaf, and stem tissue at a much higher level than in fruits and head or flower vegetables (e.g., broccoli, artichokes, cauliflower, etc.) [5].
Wash your hands after working in the garden and before washing produce.
Make sure to thoroughly wash any produce from the garden with cold running water, as lead can be present on the outside of things like root vegetables.
Limit tilling as air pollution accumulates on the top 1-2 inches of soil.
Determine which crops are poor accumulators of heavy metals, as crop type has shown to be a better predictor of metal contamination than soil [6].

Conclusions

The goal of this blog is not to scare people away from gardening, but to point out that because something is home-grown does not mean it will be safe for consumption. Taking steps to prevent or reduce heavy metal contamination in the garden will result in healthier produce and reduced exposure to toxins. As a follow-up, ZRT Laboratory offers heavy metal and essential element testing in both blood and urine, which will help identify if recent/past exposure has occurred.

Related Resources

References

[1] Mench, M, et al.Evaluating of metal mobility, plant availability and immobilization by chemical agents in a limed-silty soil. Environmental Pollution, 1004;86:279–286.

[2] Säumel I, et al. How healthy is urban horticulture in high traffic areas? Trace metal concentrations in vegetable crops from plantings within inner city neighbourhoods in Berlin, Germany. Environ Pollut. 2012;165:124-32.

[3] Gherardi M, et al. Heavy metals in the soil-plant system: monitoring urban and extra-urban parks in the Emilia Romagna Region (Italy). Agrochimica 2009;53:196–208.

[4] Sauvé S, et al. Solid-solution partitioning of metals in contaminated soils: Dependence on pH, total metal burden, and organic matter. Environ Sci Technol. 2000;34:1125–1131.

[5] Cheng S., et al. Efficiency of constructed wetlands in decontamination of water polluted by heavy metals. Ecological Engineering. 2002;18:317-325.

[6] Alexander PD, et al. Genotypic variations in the accumulation of Cd, Cu, Pb and Zn exhibited by six commonly grown vegetables. Environ Pollut. 2006;144:736-45.

Where Does Dietary Iodine Come From?

Thu, 09 May 2019 13:49:55 -0700

Have you ever wondered where dietary iodine comes from? Most people are familiar with iodized salt and shellfish containing high levels of iodine, but few realize a vast assortment of food and drinks contain this essential nutrient.

What Food Products Contain the Highest Levels of Iodine?

It may come as a surprise that most dietary iodine comes from dairy products such as milk, cheese and yogurt. Iodine is used to prevent bacteria growth in cattle feed and it can also be used as a sanitizer when milking cows. Because cows typically graze in fields during the summer and feed inside during the winter, iodine levels in dairy products vary quite considerably and can be higher during the winter [1][2][3]. On average, one cup of milk provides 56 µg iodine [4].

Marine products such as seafood and seaweed can be very rich in iodine; the concentration of iodine in the ocean is around 60 µg/L [5]. Marine fish iodine content ranges from 2 µg/100 g to more than 1000 µg/100 g wet tissue, with cod containing the highest amount [6]. Seaweed iodine content can range from 16 µg/g in a sheet of nori to over 8000 µg/g in kelp granules, based on dry weight [7]. There are many things to consider when estimating iodine content of seaweeds, including species, dry or wet weight, time of year, water quality, and cooking style.

Bread and cereal used to contain high levels of iodine when it was used as a conditioner; bread iodine levels averaged 150 µg a slice [3]. However, many bakeries now use bromine instead of iodine as a dough conditioner [4].

Another great source of iodine is eggs. Iodine content varies depending on the location and feed; iodine content should be about 25 µg/egg [4]. Egg yolks contain a much higher amount of iodine (around 5x) than do egg whites [8].

What Are Some Other Common Food Sources with Iodine?

The National Institutes of Health has created a list of foods containing iodine.

What Diet Trends Are Becoming More Common and How Does that Affect Our Iodine Intake?

Iodine intake may possibly be on the decline in the US due to government recommendations and health trends that are growing in popularity.

The Departments of Agriculture and Health and Human Services are asking over half of the US population (those who are at risk of higher blood pressure, i.e., people who are over 50 or African American) to reduce their recommended daily intake (RDI) of 2.3 g sodium a day to around 1.5 g a day [9]. Iodized salt in the US contains 77 µg iodine/g. Assuming the use of iodized salt and daily consumption of the RDI, that is a loss of 62 µg of iodine a day, which has a significant impact on iodine levels in the body.

Less milk is consumed today than it was 50 years ago. The consumption of milk in gallons per person per year dropped from 30 in 1968 to 19 in 2008 [10]. Since milk is one of the largest sources of dietary iodine, this decline lowers the overall dietary iodine intake in the US. Also, a health trend to lower cholesterol has resulted in an increase in consumption of egg whites instead of whole eggs, thereby eliminating the high-iodine yolk.

If the body does not get enough iodine, thyroid hormone synthesis is impaired and thyroid-related problems can occur (hypothyroidism, goiter).

Why Do We Need Iodine in Our Diet?

Iodine is required primarily for thyroid hormone synthesis and is the main constituent of the thyroid hormones thyroxine [T4] and triiodothyronine [T3]. If the body does not get enough iodine, thyroid hormone synthesis is impaired and thyroid-related problems can occur (hypothyroidism, goiter).

How Does the Body Utilize Dietary Iodine?

When the body digests food products, iodine absorption occurs in the stomach and small intestine for 1-2 hours, and the circulating iodine is taken up by the thyroid and other cells in the body [11][12]. Around 97% of the dietary iodine not taken up by the thyroid or other cells is excreted in the urine, with the remainder in sweat, tears, saliva, and feces [13]. Absorption of dietary iodine by the thyroid can be twice as high in people who are iodine deficient [14].

How Do I Know If I Am Getting Enough Iodine in My Diet?

The recommended daily intake for adults (non-pregnant) is 150 µg of iodine a day. If you focus on consuming one or two products such as milk or whole eggs daily, eat seafood/seaweed a couple of times a week, or simply take an iodine supplement, reaching 150 µg a day will not be an issue. By testing iodine levels in urine, you can approximate how much iodine is consumed daily. ZRT Laboratory has developed a simple dried urine test for iodine as well as selenium, an essential mineral for thyroid hormone synthesis.

Related Resources:

References:

[1] Dahl L, et al. Iodine concentration in Norwegian milk and dairy products. Br J Nutr 2003; 90: 679-85.

[2] Hemken RW. Factors that influence the iodine content of milk and meat: a review. J Anim Sci 1979; 48, 981–985.

[3] Pearce EN, et al. Sources of dietary iodine: bread, cows’ milk, and infant formula in the Boston area. J Clin Endocrinol Metab 2004;89:3421– 4.

[4] Pennington JAT, et al. Composition of core foods of the U.S. food supply, 1982–1991. J Food Comp Anal. 1995; 8:171–217.

[5] Wong, GTF. The marine geochemistry of iodine. Rev. Aquat. Sci. 1991; 4:45–73.

[6] Souci SW, et al. Food Composition and Nutrition Tables 1986, Wissenschafliche Verlagsgesellschaft GmbH, Stuttgart, Germany.

[7] Teas J, et al. Variability of iodine content in common commercially available edible seaweeds. Thyroid. 2004;14:836–841.

[8] Haldimann M, et al. Iodine content of food groups. J Food Comp Anal 2005; 18:461–471

[9] Gardner, Amanda. "New U.S. Dietary Guidelines Focus on Salt Reduction." US News . N.p., 31 Jan. 2011. Web. 20 Apr. 2011.

[10] Dairy Today Editors. "Total U.S. Milk Consumption Continues to Drop, But Demand for Lowfat Milk Grows." AgWeb. N.p., 4 Oct. 2010. Web. 20 Apr. 2011.

[11] Aurengo A, et al. Adaptation of thyroid function to excess iodine (in French). Presse Médicale 2002; 31: 1658-63.

[12] Verger P, et al. Iodine kinetics and effectiveness of stable iodine prophylaxis after intake of radioactive iodine: a review. Thyroid 2001; 11:353-361.

[13] U.S. Department of Health and Human Services. Toxicological profile for iodine. Agency for Toxic Substances and Disease Registry 2004.

[14] Zanzonico PB, Becker D. Effects of time of administration and dietary iodine levels on potassium iodide (KI) blockade of thyroid irradiation by 131I from radioactive fallout. Health Phys 2000 ; 78 : 660 – 7.

Cadmium in Jewelry - Not All That Glitters is Gold

Thu, 02 May 2019 18:52:58 -0700

When shopping for jewelry, do you consider what metals make up earrings, bracelets, rings, and other shiny items? A report by the Center for Environmental Health (CEH) in California detailed that cadmium was present in numerous jewelry items tested from stores including Ross, Walgreens and Nordstrom Rack [1]. The amount of cadmium, a toxic heavy metal, ranged from 40-100% in the items testing positive.

Is Cadmium Allowed in Jewelry?

Surprisingly, there are no restrictions on the amount of cadmium allowed in adult jewelry in the United States. There is a limit of 0.03% cadmium in children’s jewelry in California, a result of a settlement in 2011, after it was found at high levels in jewelry marketed toward pre-teens [2]. Children are more likely to be exposed to cadmium in jewelry as they might swallow or chew on the metal pieces. The European Commission banned cadmium in all jewelry sold in Europe starting in 2011 [3].

Why is Cadmium in Jewelry?

At some point cadmium became a popular replacement for lead in jewelry, likely due to an increase in lead restrictions. Cadmium is used to add mass and weight to jewelry and can add a shiny finish. Cadmium has a lower melting point than metals such as zinc, reducing the energy required to melt it into shape.

The Agency for Toxic Substances and Disease Registry (ATSDR) lists cadmium as the number 7 most significant threat to human health

Why is Cadmium Dangerous?

Cadmium is a dangerous heavy metal and a known carcinogen [4]. The Agency for Toxic Substances and Disease Registry (ATSDR) lists cadmium as the number 7 most significant threat to human health, based on its frequency, toxicity, and potential for human exposure [5]. Cadmium has a half life in the body around 10-30 years, meaning that a single exposure event can stick around for nearly a lifetime. As we age, cadmium body burden slowly increases. Cadmium primarily targets kidneys and bones, but can also be detrimental to reproductive health. Although inhalation is the most dangerous route of exposure (10-50% absorption), ingestion (2.5-5% absorption) and dermal (0.5% absorption) exposure are also dangerous, especially at high concentrations [6].

How do I Protect Myself?

There is no simple way to tell if jewelry contains cadmium or not just by looking at it. Buying jewelry that is made locally or its metal content verified by the retailer can reduce the risk of cadmium exposure. Non-metal decorative items such as ceramic, leather, plastic, or fiber can be worn instead. ZRT Laboratory offers two ways to test for exposure to cadmium. Whole blood cadmium is the best indicator of recent exposure (months), while urine cadmium is the best indicator of long term exposure (years). Overall, it is best to avoid any exposure to cadmium, as it will surely stick around for a long period of time.

Related Resources

References

[1] https://www.ceh.org/news-events/press-coverage/content/ap-exclusive-toxic-metal-found-chain-stores-jewelry/

[2] https://www.ceh.org/legacy/storage/documents/cadmium_report_2_2010.pdf

[3] http://europa.eu/rapid/press-release_IP-11-620_en.htm

[4] https://www.atsdr.cdc.gov/phs/phs.asp?id=46&tid=15

[5] https://www.atsdr.cdc.gov/spl/

[6] https://www.atsdr.cdc.gov/csem/csem.asp?csem=6&po=9

Gadolinium – A Toxic Rare-Earth Element That Isn’t So Rare

Thu, 18 Apr 2019 12:38:56 -0700

Gadolinium is a rare-earth heavy metal that most humans will have little exposure to. The designation of “rare-earth” element is misleading as it has a very common medical use: gadolinium-based contrast agents (GBCAs). GBCAs were first approved in 1988 to help make diseased tissues look brighter or darker during Magnetic Resonance Imaging (MRI). In 2017 nearly 40% of MRIs used GBCAs, and it is estimated that over 450 million GBCAs have been administered worldwide since 1988 [1]. While most gadolinium is flushed from the body following an MRI exam, new research suggests extended retention in multiple organs, leading to potential health issues.

GBCAs and MRIs

Gadolinium is bound to a ligand (an ion or molecule that binds metals) to create the GBCA. It is believed this chelated form of gadolinium is non-toxic and has a very short half-life in the body. There are two types of GBCA; linear and macrocyclic. Macrocyclic GBCAs cage gadolinium in the ligand while linear GBCAs do not. The stability of GBCAs isn’t completely related to its structure. Typically, extra ligand needs to be added to linear GBCAs during storage to prevent the release of free gadolinium, while macrocyclic GBCA can be stored without additional ligand. Each GBCA is chosen based on the tissue or organ being examined. Macrocyclic GBCAs are excreted in urine while linear GBCAs are excreted in urine or urine/bile. GBCAs have a half-life of about 1.5 hours if renal function is normal, and around 90% of the total dose is excreted in 12 hours [2][3][4]. A single dose of GBCA contains 1-2 g of gadolinium [5].

Release of Gadolinium from GBCAs

A study showed that gadolinium can be released from linear GBCAs, but not macrocyclic GBCAs, in serum at 37 °C (body temperature) [6]. Metals such as zinc, copper, and iron have a high affinity for the ligand bound to gadolinium and can increase the release of gadolinium from GBCAs [3]. Ligands such as phosphate and carbonate can also increase the release of gadolinium. The accumulation of gadolinium in tissues is often associated with the presence of zinc, calcium, phosphorus and iron [7][8][9].

Free gadolinium can block calcium channels and inhibit nerve transmissions, muscle contraction, blood coagulation, and mitochondrial function.

Gadolinium Toxicity and Nephrogenic Systemic Fibrosis

Free gadolinium (Gd³⁺) is a very toxic heavy metal because its ionic radius is very similar to that of calcium. Free gadolinium can block calcium channels and inhibit nerve transmissions, muscle contraction, blood coagulation, and mitochondrial function [10][11][12][13]. Gadolinium can also replace calcium in bone [14]. Studies on rats showed that only 1-3% of injected free gadolinium is excreted daily with a majority deposited in bone, kidney, and liver [15]. Even though GBCAs are considered safe, there is still the possibility that some of the dose will de-chelate to free gadolinium, especially with linear GBCAs. A condition called Nephrogenic Systemic Fibrosis (NSF) was linked to the use of GBCAs in patients with renal insufficiency. NSF results in free gadolinium accumulation in the kidney, heart, bones, lungs, and skin, usually resulting in death [16]. The half-life of GBCAs is significantly increased in renally impaired patients, resulting in a greater release of free gadolinium due to the contrast agent remaining in the body for a longer period. The onset of symptoms from NSF is usually weeks to months, but in some cases has occurred years after administration [17]. Once this connection was made, screening for renal insufficiency became an important part of GBCA administration. There has been a major shift moving away from linear GBCAs due to de-chelation concerns [18].

Environmental Contamination

Gadolinium accumulation in aquatic environments is concerning. High levels of administered GBCAs are excreted in urine and flushed down the toilet, especially at hospitals. Gadolinium is only partially removed during water treatment, and there is concern that the treatment process may de-chelate gadolinium from its ligand. A study looking at waste water released into aquatic environments around hospitals measured gadolinium levels from 100-1000 µg/L in surface water (normal background is 1-4 ng/L) [19]. Another study showed that surface water gadolinium in San Francisco Bay has increased 10-fold in 20 years [20].

New Research: Gadolinium Accumulation in Brain and FDA Warning

New research using autopsy specimens from patients receiving GBCAs in 2015-2016 revealed gadolinium accumulation in brain tissue [21][22][23]. Deposition in the brain can occur with both macrocyclic and linear GBCAs, but linear GBCAs seem to deposit more gadolinium [24]. It is still unclear whether gadolinium is in the free or chelated form and how it is transferred to the brain. The Pharmacovigilance and Risk Assessment Committee of the European Medicines Agency recommended the discontinuation of four linear GBCAs in 2017 [25]. The FDA acknowledged that GBCAs are retained in the body, including the brain, requiring new patient medication GBCA guides to help inform patients.

Gadolinium Deposition Disease

A small percentage of patients claim to have symptoms similar to those seen with Nephrogenic Systemic Fibrosis following GBCA administration. These symptoms are more frequently reported in patients receiving multiple GBCAs in a short period of time. This has been coined Gadolinium Deposition Disease (GDD), and symptoms include thick skin, digestive problems, headaches, brain fog, hearing and vision irregularities, burning sensation, itchy skin, hair loss, nausea, and trouble breathing. A patient advocate group, The Lighthouse Project was created in an “effort to increase awareness of the effect of Gadolinium Toxicity.”

Testing for Gadolinium

Natural gadolinium exposure is very rare and most people that have never received a GBCA will only show trace levels in urine. Urine is the best marker for gadolinium as it is primarily excreted via the kidneys, and because it is rapidly cleared from blood circulation so blood levels are not a good indicator of gadolinium retention in the body. Urine gadolinium levels are very high after GBCA administration, and gradually drop close to zero after many years. Gadolinium excretion is highly correlated with the time passed since the last GBCA administration, but some people excrete it faster or slower than others. ZRT Laboratory offers a dried urine test for gadolinium along with other heavy metals that is sensitive into the low parts per trillion (PPT).

Related Resources

References

[1] Barker PB, et al. Retention Concerns About MR Studies Using Gadolinium-Based Contrast Agents. J Am Coll Radiol. 2018;15:934-936.

[2] Baker JF, et al. Pharmacokinetics and safety of the MRI contrast agent gadoversetamide injection (OptiMARK) in healthy pediatric subjects. Invest Radiol 2004;39:334–339.

[3] Weinmann HJ, et al. Pharmacokinetics of GdDTPA/dimeglumine after intravenous injection into healthy volunteers. Physiol Chem Phys Med NMR 1984;16:167–172.

[4] McLachlan SJ, et al. Pharmacokinetic behavior of gadoteridol injection. Invest Radiol 1992;27( Suppl 1):S12–15.

[5] Möller P, et al. Anthropogenic Gd in surface water, drainage system, and the water supply of the city of Prague, Czech Republic. Environ Sci Technol. 2002;36:2387-94.

[6] Frenzel T, et al. Stability of gadolinium‐based magnetic resonance imaging contrast agents in human serum at 37 degrees C. Invest Radiol 2008;43:817–828.

[7] Abraham JL, et al. Dermal inorganic gadolinium concentrations: evidence for in vivo transmetallation and longterm persistence in nephrogenic systemic fibrosis. Br J Dermatol 2008;158:273–80.

[8] Schroeder JA, et al. Ultrastructural evidence of dermal gadolinium deposits in a patient with nephrogenic systemic fibrosis and end-stage renal disease. Clin J Am Soc Nephrol 2008;3:968–75.

[9] Thakral C, Abraham JL. Gadolinium-induced nephrogenic systemic fibrosis is associated with insoluble Gd deposits in tissues: in vivo transmetallation confirmed by microanalysis. J Cutan Pathol 2009;36:1244–54.

[10] Quarles LD, et al. Aluminum-induced DNA synthesis in osteoblasts: mediation by a G-protein coupled cation sensing mechanism. J Cell Biochem 1994;56:106–17.

[11] Pałasz A, Czekaj P. Toxicological and cytophysiological aspects of lanthanides action. Acta Biochim Pol 2000;47:1107–14.

[12] Feng X, et al. Impaired mitochondrial function and oxidative stress in rat cortical neurons: implications for gadoliniuminduced neurotoxicity. Neurotoxicology 2010;31:391–98.

[13] Xia Q, et al. Gadolinium-induced oxidative stress triggers endoplasmic reticulum stress in rat cortical neurons. J Neurochem 2011;117:38–47.

[14] Vidaud C, et al. Bone as target organ for metals: the case of f-elements. Chem Res Toxicol. 2012;25:1161-75.

[15] Wedeking P, Tweedle M. Comparison of the biodistribution of 153Gd‐labeled Gd(DTPA)2‐, Gd(DOTA)‐, and Gd(acetate)n in mice. Int J Radiat Appl Instrum B 1988;15:395–402.

[16] Kay J, et al. Case records of the Massachusetts General Hospital. Case 6‐2008. A 46‐year‐old woman with renal failure and stiffness of the joints and skin. N Engl J Med 2008;358:827–838.

[17] Larson KN, et al. Nephrogenic Systemic Fibrosis Manifesting a Decade After Exposure to Gadolinium. JAMA Dermatol. 2015;151:1117-20.

[18] Runge VM. Safety of the Gadolinium-Based Contrast Agents for Magnetic Resonance Imaging, Focusing in Part on Their Accumulation in the Brain and Especially the Dentate Nucleus. Invest Radiol. 2016;51:273-9.

[19] Kümmerer K, Helmers E. Hospital effluents as a source of gadolinium in the aquatic environment. Environ Sci Technol. 2000;34:573–577.

[20] Barker PB, et al. Retention Concerns About MR Studies Using Gadolinium-Based Contrast Agents. J Am Coll Radiol. 2018;15:934-936.

[21] McDonald RJ, et al. Intracranial gadolinium deposition after contrast-enhanced MR imaging. Radiology 2015;275:772–82.

[22] Kanda T, et al. Gadolinium-based contrast agent accumulates in the brain even in subjects without severe renal dysfunction: evaluation of autopsy brain specimens with inductively coupled plasma mass spectroscopy. Radiology 2015;276:228–32.

[23] Murata N, et al. Macrocyclic and other non-group 1 gadolinium contrast agents deposit low levels of gadolinium in brain and bone tissue: preliminary results from 9 patients with normal renal function. Invest Radiol 2016;51:447–53.

[24] McDonald RJ, et al. Gadolinium Deposition in Human Brain Tissues after Contrast-enhanced MR Imaging in Adult Patients without Intracranial Abnormalities. Radiology. 2017;285:546-554.

[25] Gadolinium Toxicity. 2017. European group recommends to stop using 4 linear GBCAs. https://gadoliniumtoxicity.com/2017/03/12/ema-recommends-stop-using-linear-gbcas/

Brazil Nuts as a Selenium Supplement?

Thu, 21 Mar 2019 13:29:05 -0700

Selenium is a trace essential element that is incorporated into selenoproteins. There are at least 25 known selenoproteins in the human body, their primary roles being antioxidant enzymes such as glutathione peroxidase and thyroid deiodinases that convert thyroxine (T4) to active thyroid hormone (T3). Deficiencies in selenium can be detrimental to health, while selenium excess can be just as dangerous. Brazil nuts are commonly used as a form of selenium supplementation, but it isn’t commonly known that the level of selenium in Brazil nuts is highly variable.

Why Are Brazil Nuts High in Selenium?

Brazil nuts are well known for their high concentration of selenium. Soil conditions in parts of South America are unique in that they are deficient in sulfur, a necessary element required for the formation of the amino acids methionine and cysteine [1]. Selenium and sulfur are chemically very similar, so plants take up selenium in place of sulfur, forming the amino acids selenomethionine and selenocysteine. Soil often contains inorganic selenite and selenate, which are converted to organic selenomethionine and other methylated derivatives once taken up by the plant. Selenomethionine and selenocysteine can replace methionine and cysteine in proteins without loss of function.

Brazil nuts are well known for their high concentration of selenium; however, the amount of selenium is highly variable.

Selenium Content of Brazil Nuts

The amount of selenium in Brazil nuts is highly variable. Selenium content depends on the region in which the tree is grown, the pH of the soil, and can vary from nut to nut in a single batch or between trees [2]. According to the USDA, there is 96 µg of selenium per Brazil nut and 544 µg of selenium per serving [3]. A single serving of Brazil nuts is 28.35 grams (1 ounce), with individual nuts weighing around 5 grams. In a single study, Brazil nut selenium concentration ranged from 0.03 to 512 µg/g, a substantial difference [4]. At the highest concentration, a single serving of Brazil nuts (around 6 whole nuts) could result in a selenium intake of 14515 µg, much higher than the recommended daily amount (RDA) of 55 µg [5].

Adapted from [2][3].

Daily Recommended Selenium Intake

The Institute of Medicine’s Food and Nutrition Board set a recommended dietary allowance of 55 µg selenium/day for adults with a tolerable upper intake level of 400 µg selenium/day [6]. Higher levels of selenium intake in the range of 200-300 µg/day are believed to be effective in the prevention of certain types of cancer such as lung, colon and prostate [7][8]. Adverse effects of selenium intake are seen above 1500 µg/day, with “selenosis” and DNA damage occurring above 3000 µg/day [9][10]. Selenium toxicity can result in hair loss, tremors, kidney failure, cardiac failure, neurological and gastrointestinal issues, respiratory distress and even death [6][11]. Due to the large variation of selenium in Brazil nuts, it is difficult to determine if Brazil nuts are providing inadequate, adequate, or excessive intake.

Brazil Nut Consumption and Antioxidant Levels

In a New Zealand study, 59 adults were separated into three groups, receiving either Brazil nuts (2 nuts a day or an estimated 100 µg selenium/day), selenomethionine tablets (100 µg selenium/day), or placebo tablets (no selenium) for 3 months [12]. Plasma selenium, plasma glutathione peroxidase (a selenium-containing antioxidant) and whole blood glutathione peroxidase were measured. Plasma selenium increased by 64%, 61% and 8%; plasma glutathione peroxidase by 8%, 5% and 1.2%; and whole blood glutathione peroxidase by 13%, 5% and 1.9%, in the Brazil nut, selenomethionine, and placebo groups, respectively. Brazil nuts, therefore, increase plasma selenium levels and antioxidant production in this human population.

How Much Selenium Am I Getting from Brazil Nuts?

Measuring the selenium content of Brazil nuts is complex and requires extensive digestion in the lab and time-consuming analytical procedures. Because other foods, beverages, and supplements provide selenium on top of Brazil nuts, it is best to measure total daily selenium intake. Around 50-70% of selenium ingested is excreted in urine, therefore the amount of selenium in urine is proportional to the amount ingested [13][14]. If you are planning on supplementing with Brazil nuts, it is highly recommended that you test your urine selenium levels to determine if safe levels of selenium are being consumed. ZRT Laboratory offers a urine selenium test that also measures other essential and toxic elements.

Related Resources

References

1. Pacheco AM, Scussel VM. Selenium and aflatoxin levels in raw Brazil nuts from the Amazon basin. J Agric Food Chem. 2007;55:11087-92.

2. Silva Junior EC, et al. Natural variation of selenium in Brazil nuts and soils from the Amazon region. Chemosphere. 2017;188:650-658.

3. S. Department of Agriculture, Agricultural Research Service. USDA National Nutrient Database for Standard Reference, Release 25. Nutrient Data Laboratory Home Page, 2012.

4. Chang JC, et al. Selenium content of Brazil nuts from two geographic locations in Brazil. Chemosphere. 1995;30:801-2.

5. https://ods.od.nih.gov/factsheets/Selenium-HealthProfessional/

6. Institute of Medicine, Food and Nutrition Board. Dietary Reference Intakes: Vitamin C, Vitamin E, Selenium, and Carotenoids. National Academy Press, Washington, DC, 2000.

7. Combs GF Jr. Considering the mechanisms of cancer prevention by selenium. Adv Exp Med Biol. 2001;492:107-17.

8. Rayman MP. Selenium in cancer prevention: a review of the evidence and mechanism of action. Proc Nutr Soc. 2005;64:527-42.

9. Reid ME,. A report of high-dose selenium supplementation: response and toxicities. J Trace Elem Med Biol. 2004;18:69-74.

10. Whanger PD. Selenium and its relationship to cancer: an update. Br J Nutr. 2004;91:11-28.

11. Sunde RA. Selenium. In: Bowman B, Russell R, eds. Present Knowledge in Nutrition. 9th ed. Washington, DC: International Life Sciences Institute; 2006:480-97.

12. Thomson CD, et al. Brazil nuts: an effective way to improve selenium status. Am J Clin Nutr. 2008;87:379-84.

13. Suzuki K. Metabolomics of selenium: Se metabolites based on speciation studies. Journal of Health Science. 2005;51:107-14.

14. Sanz Alaejos M, Díaz Romero C. Urinary selenium concentrations. Clin Chem. 1993;39:2040-52.

Crystal Glassware and Wine – An Unexpected Source of Lead

Thu, 13 Dec 2018 18:56:23 -0800

Lead is everywhere. It was commonly used in paint, gasoline, plumbing pipes, jewelry, bullets, fishing weights, glazes, and cosmetics. Some regulations are now in place to eliminate lead’s incorporation into these products, but in many cases, it is still being used. I watched a special on wine in Washington State, and the host explained why leaded crystal glasses are ideal for tasting because of the way they refract light, how thin they are, and how the rough surface helps aerate wine. I had no clue that “crystal glassware” likely contains lead. With a bit of digging I found that most wine glasses and decanters contain lead, and many are still being sold this way.

Leaded Crystal Overview

Leaded crystal glassware is known for its shimmer, clarity, weight, and strength. These properties are due to the substitution of lead for calcium in glass (this also happens in our guts). Lead allows the glass to be formed at lower temperature with fewer bubbles, making it easier to work with. The history of leaded glassware goes all the way back to a recipe for lead glaze in a 1700 BC Babylonian tablet [1]. Leaded crystal, which contains around 24% lead, is often referred to as “crystal glassware,” just as dental fillings that consist of >50% mercury are called “silver fillings.” Not all crystal contains lead, as some glass manufacturers now use zinc and magnesium instead. After use, leaching of elements like lead from the glass surface leaves the crystal rough and pitted, allowing for better aeration of beverages when agitated.

The FDA recommended that lead crystal should not be used every day for wine consumption.

Leaching Lead from Crystal

The first thing that came to my mind when initially hearing “leaded crystal” was, “What amount of lead can be leached from the glass?” Digging into the literature, most scientific studies on leaching of lead from crystal were completed in the 1990s, around the same time the dangers of lead exposure were becoming evident. Around this time the FDA recommended that lead crystal should not be used every day for wine consumption [2]. They also mentioned that women of childbearing age should not use leaded crystal, and that no food or drink should be stored in crystal vessels. To update you on the health risks associated with lead, it has now been established that there is no safe level of lead exposure, especially for children (children absorb 30-75% of lead ingested while adults absorb around 10%) [3][4]. Highly acidic drinks such as soda, fruit juices, sweet tea, spirits, and wine will leach lead out of glass quicker than neutral or alkaline drinks. Since most people do not drink orange juice out of a crystal glass, literature searches were focused on wine and spirits.

Here are some findings from studies on lead leaching from crystal glasses and decanters:

Port wine kept in a leaded crystal decanter had a lead concentration of 3518 µg/L after 4 months [5].
Spirits stored in leaded crystal decanters long term had lead concentrations up to 21,530 µg/L [3].
Sherry, port and scotch whiskey stored in leaded crystal decanters reached concentrations of 1200 µg/L after 6-8 weeks, with some reaching >1000 µg/L after a couple of days [6].
Wine elutes small amounts of lead from leaded crystal in minutes [3].
During a 30-min period of wine storage in leaded crystal glass, 50% of the total lead leached occurred within one minute [7].
Repeat wine leaching experiments show that less lead is leached with each consecutive glass poured, and that cleaning of the glasses may expose new areas for lead to be leached [4].

Lead in Wine

Wine itself can be a major source of lead. The International Organization of Vine and Wine set a maximum acceptable limit of 150 µg/L lead in wine [8]. For reference, the EPA limits lead in drinking water to a maximum of 15 µg/L [9]. Lead contamination comes primarily from lead in soil (leaded gasoline being a big factor), fertilizers, and wine equipment [10]. Some wine cap foils used to be made of lead, but were phased out in the 1980s. A major study showed that international wines (red and white) had average lead levels of around 34 µg/L, while wines from the United States were much lower in lead content at around 4.4 µg/L [11].

How Much Lead Are We Talking About?

It is difficult to determine the amount of lead you are exposed to from crystal glassware and wine. Many factors such as timing, acidity, age of leaded crystal, type of leaded crystal, how it was cleaned, how many repeated uses, how it was stored, and the wine itself will cause exposures to vary. Daily lead intake assessments from older studies cannot be compared to what we see today, as lead use has dropped significantly and has been banned from products like gasoline, paint and pipes. Not too long ago, blood lead levels <100 µg/dL were considered normal, and now levels >5 µg/dL require intervention (>2 µg/dL is being considered). The most recent guideline set by the FDA states that Interim Reference Level (IRL) for lead intake is 3 µg/day for children and 12.5 µg/day for adults [12]. These numbers are 10x less than what it would take to reach blood lead action levels of 5 µg/dL in children and 10 µg/L in adults. From what I understand, a wine high in lead will put you over the IRL after drinking one glass, while lead from leaded crystal can significantly add to that amount. One sip of whiskey from a leaded crystal decanter can equate to months’ worth of exposure in a single day.

Reducing Lead Exposure

The primary route of lead exposure is through ingestion [13]. Data from the National Health and Nutrition Examination Survey (NHANES) showed that the average wine drinker consumes around 1.5 glasses of wine per day [6]. It is hard to tell the amount of lead in individual wines without laboratory testing, or the amount of lead that will be leached from leaded crystal, but there are a number of things that can help reduce lead exposure:

Buy and use non-leaded crystal or glass. I recently emailed Riedel Glass Company about leaded crystal, and they mentioned that they have discontinued the sale of leaded crystal.
New leaded crystal should be soaked in vinegar (very acidic) for 24 hours and rinsed thoroughly to leach as much lead as possible before use [11].
Wash leaded crystal by hand with a mild detergent (neutral pH), as dishwashers erode the glass, allowing for more lead to be leached [13].
If you decide to use leaded crystal, only use it for serving, never for storage [14]. This especially holds true for decanters, which hold wine and spirits for an extended period.
Instead of using decanters and leaded crystal to aerate wine, use an alternate aeration device that attaches to the wine bottle or glass.
Drink wine with a meal. A study showed that lead absorption on an empty stomach was 34%, while it was only 2.3% when consumed with a meal [15].
Consume domestic wines rather than international ones.

Takeaway Message

The point of this blog post is not to scare people away from drinking wine, but instead help people make smart choices about ways to reduce lead exposure. Blood lead levels, the standard for monitoring lead exposure, have dropped significantly over the last 50 years. This is a result of understanding the dangers of lead and removing it from things like gasoline, paint, and plumbing pipes. I am happy to hear that glass manufacturers are following suit. Some say lead from leaded crystal is harmless due to low exposure, but the reality is that no amount of exposure is safe. In 2016, lead exposure accounted for >60% of developmental intellectual disability according to The Institute for Health Metrics and Evaluation (IHME) [16]. A 2018 study that tracked >14,000 adults showed that nearly 400,000 deaths/year can be attributed to lead exposure, a level 10x higher than previously estimated [17]. There is no doubt that we are exposed to lead every day, but with knowledge of where that lead is coming from, better decisions can be made that will influence our long term health and well-being.

If you think you have been exposed to too much lead or other heavy metals, there’s a simple way to find out. Only a few drops of blood from your finger-tip or a urine collection may give you the answer. For more information about ZRT Laboratory’s dried blood spot and urine tests for lead and other heavy metals please click here.

Related Resources

References

1. Charleston, R. J. (1960), LEAD IN GLASS. Archaeometry, 3: 1-4.

2. https://www.nytimes.com/1991/02/20/garden/fda-issues-warnings-on-using-lead-crystal.html.

3. US Environmental Protection Agency. Air quality criteria for lead. Research Triangle Park, NC, 1986 (Report EPA-600/8-83/028F).

4. Drill S et al. The environmental lead problem: an assessment of lead in drinking water from a multi-media perspective. Washington, DC, US Environmental Protection Agency, 1979 (Report EPA-570/9-79-003).

5. Graziano JH, Blum C. Lead exposure from lead crystal. Lancet. 1991;337:141-2.

6. Appel BR, et al. Potential lead exposures from lead crystal decanters. Am J Public Health. 1992;82:1671-3.

7. Hight SC. Lead migration from lead crystal wine glasses. Food Addit Contam. 1996;13:747-65.

8. Annex: maximum acceptable limits. In: International code of oenological practices: OIV code sheet - issue 2015/01. 2015.

9. https://www.atsdr.cdc.gov/toxfaqs/tfacts13.pdf.

10. Bora FD, et al. Vertical distribution and analysis of micro-, macroelements and heavy metals in the system soil-grapevine-wine in vineyard from North-West Romania. Chem Cent J. 2015;9:19.

11. Towle KM, et al. A human health risk assessment of lead (Pb) ingestion among adult wine consumers. Food Contamination. 2017;4(7).

12. https://www.fda.gov/food/foodborneillnesscontaminants/metals/ucm2006791.htm.

13. Agency for toxic substances and disease registry case studies in environmental medicine (CSEM) lead toxicity. 2012.

14. https://www.canada.ca/en/health-canada/services/healthy-living/your-health/products/lead-crystalware-your-health.html.

15. Gulson BL, et al. Contribution of lead in wine to the total dietary intake of lead in humans with and without a meal: a pilot study. Journal of Wine Research. 1998;9:5-14.

16. Institute for Health Metrics and Evaluation (IHME). GBD Compare. Seattle, WA: IHME, University of Washington; 2017.

17. Lanphear BP, et al. Low-level lead exposure and mortality in US adults: a population-based cohort study. Lancet Public Health. 2018;3:e177-e184.

Five Common Sources of Mercury Exposure

Fri, 27 Jul 2018 09:33:00 -0700

Mercury is one of the most toxic heavy metals. There are numerous natural and man-made sources of mercury, but the most concerning are the ones we are exposed to daily. Mercury is known to affect the nervous, circulatory, immune, reproductive, and digestive systems, along with organs such as the kidneys, lungs, and gastrointestinal tract. Mercury primarily targets sulfhydryl groups (sulfur) and selenium, for which it has a high affinity. Later in this blog is a list of the most common sources of mercury exposure, but before we get into that, it is important to distinguish the three different types of mercury and their common exposure routes.

Understanding the Different Types of Mercury

Mercury exists in the environment in three forms: elemental, inorganic, and organic (most commonly as methylmercury). The amount of mercury that we absorb and retain in our bodies depends on what type of mercury we are exposed to, as well as the dose, duration, and route of exposure. The following table shows the most common mercury exposure routes and the relative levels of exposure for each.

Elemental (Hg⁰) – less than 0.01% of elemental mercury is absorbed in the gastrointestinal (GI) tract when swallowed, but when inhaled, over 80% is absorbed by the lungs and is rapidly distributed throughout the body. Absorption of elemental mercury through the skin is poor [1]. The best marker of elemental mercury exposure is urine.

Inorganic (Hg²⁺) – the toxicity of inorganic mercury compounds depends on their solubility. These are usually present as solids, not vapors, so inhalation risk is low. Acute skin exposure can lead to dermatitis and corrosive burns. Oral consumption of inorganic mercury generally affects the kidneys through bioaccumulation, as the molecule is polar and lipophobic (fat “hating”) [1]. The best marker of inorganic mercury exposure is urine.

Organic (MeHg, EtHg) – inhalation and dermal exposure to organic mercury is extremely rare but can have devastating consequences such as blindness, deafness, and loss of consciousness. Around 95% of organic mercury is absorbed when ingested, and due to its lipophilic (fat “loving”) and non-polar nature, it can cross the blood-brain barrier [2]. The best marker of organic mercury exposure is whole blood.

Fish and Shellfish

Fish and shellfish consumption is the leading dietary source of mercury exposure. Inorganic mercury is converted to the more toxic organic methylmercury by bacteria. Methylmercury then works its way up the food chain, from small organisms to fish and shellfish, accumulating in their tissue. Fish species with the highest tissue mercury concentrations are king mackerel, shark, and swordfish at 0.73, 0.97, and 0.99 parts per million (mg per kg sample) respectively. Tuna is also known to accumulate high levels of mercury. A complete list of fish and shellfish mercury levels can be found here: http://www.fda.gov/Food/FoodborneIllnessContaminants/Metals/ucm115644.htm

Dental amalgams will continuously leach elemental mercury vapor during chewing, brushing and corrosion into saliva, which is inhaled and has been proven to accumulate in the body.

Dental Amalgams

Dental amalgams contain about 50% elemental mercury. Liquid mercury in a pre-measured capsule is mixed with silver, copper, tin, and other elements, to create the filling. Each capsule contains mercury in amounts ranging from 100 to 1000 mg. Dental amalgams are commonly called “silver” fillings because of their appearance, which can be misleading to the consumer. Dental amalgams will continuously leach elemental mercury vapor during chewing, brushing and corrosion into saliva, which is inhaled and has been proven to accumulate in the body.

Vaccines Containing Thimerosal

Thimerosal is a preservative currently used in some flu vaccinations, administered to both children and adults. Thimerosal is metabolized in the body to form ethylmercury, with each vaccination containing around 12.5-25 µg of ethylmercury per dose. Vaccinations for children only no longer contain thimerosal.

Mercury Thermometers

Mercury thermometers contain between 500 to 54,000 mg of elemental mercury. Elemental mercury vapor is easily absorbed by the body, while direct exposure of liquid mercury from a broken thermometer results in little assimilation via the GI tract. Spilled mercury from a broken thermometer beads into tiny drops, which can get into carpet and cracks and continuously release harmful mercury vapor that can be inhaled or absorbed through the skin. Mercury thermometers are nearly phased out for both medical and industrial use, but many still reside in personal medicine cabinets and need to be disposed properly (https://www.epa.gov/hw/universal-waste).

Fluorescent Light Bulbs

Fluorescent light bulbs contain less than 10 mg of mercury in elemental vapor form. Every fluorescent light bulb is required to have a Hg marking (chemical symbol for mercury) on the bulb. Because fluorescent bulbs contain mercury, they should be disposed of properly (https://www.epa.gov/hw/universal-waste) to reduce the amount of mercury released into the environment. If broken, fluorescent lights will continuously emit mercury vapor at dangerous levels.

Summary

Mercury is not safe in any form or by any route of exposure. Understanding the three types of mercury and their common exposure routes will help prevent unnecessary exposure to this dangerous heavy metal. If you are unsure of current or past exposure to mercury, a combination urine/blood mercury test can be helpful in determining the likely type of exposure. Monitoring selenium can be helpful as well, as selenium is known to bind tightly to mercury and reduce its toxicity [3] [4].

Related ZRT Resources

References

[1] Park JD, Zheng W. Human exposure and health effects of inorganic and elemental mercury. J Prev Med Public Health. 2012 Nov;45(6):344-52.

[2] National Research Council (US) Committee on the Toxicological Effects of Methylmercury. Toxicological Effects of Methylmercury. Washington (DC): National Academies Press (US); 2000. 2, CHEMISTRY, EXPOSURE, TOXICOKINETICS, AND TOXICODYNAMICS. Available from: https://www.ncbi.nlm.nih.gov/books/NBK225779/

[3] Ralston NV, Raymond LJ. Dietary selenium's protective effects against methylmercury toxicity. Toxicology. 2010 Nov 28;278(1):112-23.

[4] Spiller HA1,2. Rethinking mercury: the role of selenium in the pathophysiology of mercury toxicity. Clin Toxicol (Phila). 2018 May;56(5):313-326.

Cadmium’s Connection to Infertility and Reproduction

Thu, 14 Jun 2018 07:39:00 -0700

Cadmium is a dangerous heavy metal and a known carcinogen. Even though daily exposure is usually relatively low compared to toxins like arsenic, cadmium bioaccumulates with a half-life in the body of 25-30 years.

Essentially, the older you are, the more cadmium you have stored in your body. When cadmium exposure is high, it increases cellular oxidation products that deplete antioxidants like glutathione peroxidase and superoxide dismutase, rendering the body defenseless to further oxidative damage [1].

The most common sources of cadmium exposure are green leafy vegetables and grains, as cadmium is accumulated from contaminated water and soil. Thus, people consuming plant-based diets may be at a higher risk for cadmium exposure. Tobacco, a green leafy plant, concentrates cadmium, which is then highly absorbed through the lungs when smoked, resulting in blood cadmium levels 3 times higher than in non-smokers [2]. In comparison, only a small percentage of cadmium is absorbed in the gut from food. Other sources of cadmium include industrial activities such as smelting and refining, mining, and manufacturing of batteries and cadmium-containing pigments.

Cadmium and Reproductive Organs

Cadmium is known to accumulate in the liver and kidney (~50% of body burden), but also in reproductive organs such as the testes, ovaries, and placenta [3] [4] [5] [6]. Pregnant women tend to accumulate more cadmium than non-pregnant women, most likely due to reduced iron stores and higher gut absorption [7]. Women who smoke during pregnancy have significantly higher cord blood cadmium levels (placental burden) that correlate to blood cadmium levels [8]. Luckily, cadmium is largely retained in the placenta as it does not effectively cross the placental barrier. On the flip side, cadmium can inhibit zinc, along with other essential elements like copper, calcium, and potassium, from being transported across the placenta [9]. Cadmium accumulation in the testes has been linked to reduced fertility, as shown in studies of male metal workers with lower pregnancy rates and reduced semen quality [10] [11] [12] [13] [14] [15].

Cadmium and Reproductive Hormones

Numerous studies have been published linking cadmium to infertility and complications later in life.

Cadmium directly, and indirectly, influences reproductive hormones. Studies in rodents have shown that cadmium alters levels of testosterone, LH, and FSH, which are all essential for reproduction [16]. Acting as a metalloestrogen, cadmium mimics the growth-promoting actions of estrogens, promoting mammary gland development, inducing early puberty in females, and increasing overall lifetime breast cancer risk [17] [18] [19]. In the context of pregnancy, another study found that a 2-fold increase in placental cadmium was associated with a 50% reduction in placental progesterone [20].

Cadmium's Effect on the Fetus and Infant

Numerous studies have been published linking cadmium to infertility and complications later in life. Lower birthweight, reduced cognitive ability, epigenetic modifications, and increased chances of a miscarriage have all been associated with cadmium exposure [21] [22] [23]. Post-delivery, a newborn can be exposed to cadmium from second-hand smoke, infant formula, and breast milk.

The Zinc/Cadmium Connection

Cadmium’s [Cd²⁺] primary antagonist in the body is zinc [Zn²⁺] due to similar electron configurations. Cadmium disrupts zinc homeostasis, whereas zinc protects against cadmium toxicity [24] [25]. Zinc is essential for ovulation, egg fertilization, and the development and maturation of spermatozoa, along with many non-reproductive processes in the body [26]. One of zinc’s protective mechanisms is to stimulate metallothionein production (a zinc storage protein) which binds tightly to heavy metals like cadmium to prevent oxidative stress. With regard to reproductive function, zinc is essential for ovulation, egg fertilization, and the development and maturation of spermatozoa, along with many non-reproductive processes in the body [26]. Increased zinc supplementation was shown to prevent testicular toxicity and maintain testosterone production during cadmium-induced prostate cancer in rats [27]. It may have similar protective actions in humans. Zinc also helps prevent cadmium from disturbing bone metabolism, a result of the displacement of calcium (Ca²⁺) which has a similar atomic radius [28].

What Can You Do to Protect Against, Detect, or Prevent Cadmium Exposure?

Test for recent (whole blood) and past (urine) cadmium exposure
Refrain from smoking cigarettes or any other tobacco-containing product
Test garden soil for cadmium (and other toxic elements like lead)
Eat a varied diet high in antioxidants and essential elements (zinc/calcium/selenium/magnesium/iron are all very important)
Minimize exposure when working with commercial products (e.g., pigments) containing cadmium

More about Elements Testing

References

[1] Sen Gupta R, et al. Vitamin C and vitamin E protect the rat testes from cadmium-induced reactive oxygen species. Mol Cells. 2004;17:132-9.

[2] Toxicological Profile for Cadmium (Final Report). In: Registry AfTSaD, ed. Atlanta: ASTDR; 1999.

[3] Järup L, et al. Health effects of cadmium exposure--a review of the literature and a risk estimate. Scand J Work Environ Health. 1998;24 Suppl 1:1-51.

[4] Varga B, et al. Age dependent accumulation of cadmium in the human ovary. Reprod Toxicol. 1993;7:225-8.

[5] Piasek M, et al. Placental cadmium and progesterone concentrations in cigarette smokers. Reprod Toxicol. 2001;15:673-81.

[6] Paksy K, et al. Effect of cadmium on morphology and steroidogenesis of cultured human ovarian granulosa cells. J Appl Toxicol. 1997;17:321-7.

[7] Nishijo M, et al. The gender differences in health effects of environmental cadmium exposure and potential mechanisms. Mol Cell Biochem. 2004;255:87-92.

[8] Galicia-García V, et al. Cadmium levels in maternal, cord and newborn blood in Mexico City. Toxicol Lett. 1997;91:57-61.

[9] Kuriwaki J, et al. Effects of cadmium exposure during pregnancy on trace elements in fetal rat liver and kidney. Toxicol Lett. 2005;156:369-76.

[10] Robins TG, et al. Semen quality and fertility of men employed in a South African lead acid battery plant. Am J Ind Med. 1997;32:369-76.

[11] Bonde JP. The risk of male subfecundity attributable to welding of metals. Studies of semen quality, infertility, fertility, adverse pregnancy outcome and childhood malignancy. Int J Androl. 1993;16 Suppl 1:1-29.

[12] Gennart JP, et al. Fertility of male workers exposed to cadmium, lead, or manganese. Am J Epidemiol. 1992;135:1208-19.

[13] Chia SE, et al. Blood cadmium levels in non-occupationally exposed adult subjects in Singapore. Sci Total Environ. 1994;145:119-23.

[14] Akinloye O, et al. Cadmium toxicity: a possible cause of male infertility in Nigeria. Reprod Biol. 2006;6:17-30.

[15] Benoff S, et al. Male infertility and environmental exposure to lead and cadmium. Hum Reprod Update. 2000;6:107-21.

[16] Lafuente A, et al. Cadmium exposure differentially modifies the circadian patterns of norepinephrine at the median eminence and plasma LH, FSH and testosterone levels. Toxicol Lett. 2004;146:175-82.

[17] Johnson MD, et al. Cadmium mimics the in vivo effects of estrogen in the uterus and mammary gland. Nat Med. 2003;9:1081-4.

[18] Stoica A, et al. Activation of estrogen receptor-alpha by the heavy metal cadmium. Mol Endocrinol. 2000;14:545-53.

[19] Lin J, et al. Dietary intake and urinary level of cadmium and breast cancer risk: A meta-analysis. Cancer Epidemiol. 2016;42:101-7.

[20] Piasek M, et al. Placental cadmium and progesterone concentrations in cigarette smokers. Reprod Toxicol. 2001;15:673-81.

[21] Luo Y, et al. Maternal blood cadmium, lead and arsenic levels, nutrient combinations, and offspring birthweight. BMC Public Health. 2017;17:354.

[22] Sanders AP, et al. Perinatal and Childhood Exposure to Cadmium, Manganese, and Metal Mixtures and Effects on Cognition and Behavior: A Review of Recent Literature. Curr Environ Health Rep. 2015;2:284-94.

[23] Appleton AA, et al. Prenatal exposure to neurotoxic metals is associated with increased placental glucocorticoid receptor DNA methylation. Epigenetics. 2017;12:607-615.

[24] Brzóska MM, et al. Interactions between cadmium and zinc in the organism. Food Chem Toxicol. 2001;39:967-80.

[25] Brzóska MM, et al. Effect of zinc supplementation on bone metabolism in male rats chronically exposed to cadmium. Toxicology. 2007;237:89-103.

[26] Favier AE. The role of zinc in reproduction. Hormonal mechanisms. Biol Trace Elem Res. 1992;32:363-82.

[27] Waalkes MP, et al. Cadmium carcinogenesis in male Wistar [Crl:(WI)BR] rats: dose-response analysis of effects of zinc on tumor induction in the prostate, in the testes, and at the injection site. Cancer Res. 1989;49:4282-8.

[28] Brzóska MM, et al. Effect of zinc supplementation on bone metabolism in male rats chronically exposed to cadmium. Toxicology. 2007;237:89-103.

Is Sweating a Good Bet for Heavy Metal Detox?

Thu, 08 Mar 2018 08:30:00 -0800

A couple years back, I wrote a blog about iodine deficiency in athletes resulting from excessive sweat loss.

Later, while studying the kinetics of the iodine loading test which involves taking a 50-mg dose of iodine and collecting urine for 24 hours, I investigated the excretion of iodine in sweat along with urine.

Surprisingly iodine levels in sweat tracked urine iodine excretion over a period of 3 days. The goal was to show that the loss of iodine through sweat can represent a significant portion of the 50-mg dose, something the creators of the Iodine Loading Test had not accounted for.

As time went on at ZRT, we expanded our elements testing to include the “big 4” heavy metals arsenic, cadmium, lead, and mercury. These heavy metals have very different half-lives and excretion routes.

Literature is rather limited on the subject of heavy metal elimination through sweat, but with the advancement of sweat collection and sophisticated instrumentation, recent studies have shown encouraging results on heavy metal detox via sweat.

An Interesting Sweat Study

A study by Genuis and colleagues looked at serum, urine, and sweat levels of toxic heavy metals and essential elements and found compelling results. [1] The most striking result was the large excretion of lead and cadmium in sweat collected during exercise or in an infrared/steam sauna in comparison to concurrent serum and urine collections. Interestingly, lead and cadmium are elements characterized by long half-lives in the body (20-30 years), miniscule excretion in urine, and serious bioaccumulation. A typical sauna session results in a half-liter of sweat loss, meaning that a significant amount of toxins are potentially being excreted. [2] Other studies have shown similar results. [3] [4] [5] This means that a possible route of detoxing from lead and cadmium may be through sweat.

So, Heavy Metals are Excreted Through Sweat?

Possibly.

Regardless of how heavy metals are excreted, it is well known that essential elements are lost while sweating.

Even though studies have shown that sweat excretion of heavy metals should not be overlooked, I am somewhat critical of the collection methodologies used in different studies. An investigation into drugs of abuse in sweat showed that blood capillaries and adipose tissue may contribute to secretions from sebaceous and apocrine glands connected to hair follicles. [6] These are different than the eccrine sweat glands which are the main producers of sweat for thermal regulation. Most sweat collection studies involve scraping the skin to collect sweat, which will also pick up fatty sebum excretions (disintegrated epithelial cells).

Most toxins, including heavy metals, are fat-soluble. It is plausible that sebum excretions from the sebaceous gland are a route of heavy metal buildup and excretion that may stick around longer than sweat from the eccrine gland, which quickly evaporates. This is one of the reasons why hair testing is difficult to control, because hair follicles coated with sebum (think oily excretion) is either washed away or left unwashed depending on the laboratory protocol, leading to large variations in results. [7]

Eccrine Sweat Glands: Present across the entire body with highest concentrations in the palms of hands and soles of feet. Open up directly to skin surface.

Apocrine Sweat Glands: Located only where hair follicles are present in armpits, ears, eyelids, perineum, and areola, from puberty on.

Sebaceous Glands: Located across the entire body, minus the palms of hands and soles of feet. They primarily open up into hair follicles, but some open directly to the skin surface. They are most abundant in the scalp and face.

Conclusion

At this point it is difficult to tell if heavy metals are excreted through eccrine sweat glands or apocrine sweat glands, or the sebum from sebaceous glands, or all of the above. It is also possible that sweat samples used in the studies mentioned were contaminated by dermal exposure to heavy metals. Future studies monitoring sweat should compare collections from areas where sebaceous glands are present in high concentrations (scalp and face) to areas where only eccrine sweat glands are present (palms and soles).

It is also unclear whether essential elements like iodine behave the same way as heavy metals when it comes to sweat excretion. The iodine sweat collection study I mentioned at the beginning of this blog post involved scraping the sweat off the skin of my arm and forehead, places where both eccrine and sebaceous glands are present.

Regardless of how heavy metals are excreted, it is well known that essential elements are lost while sweating, so it is important to replenish lost nutrients when exercising or using a sauna.

More about Elements Testing

References

[1] Genuis SJ, Birkholz D, Rodushkin I, Beesoon S. Blood, urine, and sweat (BUS) study: monitoring and elimination of bioaccumulated toxic elements. Arch Environ Contam Toxicol. 2011;61(2):344-57.

[2] Hannuksela ML, Ellahham S. Benefits and risks of sauna bathing. Am J Med. 2001;110(2):118-26.

[3] Sheng J, Qiu W, Xu B, Xu H, Tang C. Monitoring of heavy metal levels in the major rivers and in residents' blood in Zhenjiang City, China, and assessment of heavy metal elimination via urine and sweat in humans. Environ Sci Pollut Res Int. 2016;23(11):11034-45.

[4] Tang S, Yu X, Wu C. Comparison of the Levels of Five Heavy Metals in Human Urine and Sweat after Strenuous Exercise by ICP-MS. Journal of Applied Mathematics and Physics. 2016; 4:183-188.

[5] Omokhodion FO, Howard JM. Trace elements in the sweat of acclimatized persons. Clin Chim Acta. 1994;231(1):23-8.

[6] Levisky JA, Bowerman DL, Jenkins WW, Karch SB. Drug deposition in adipose tissue and skin: evidence for an alternative source of positive sweat patch tests. Forensic Sci Int. 2000;110(1):35-46.

[7] Chittleborough G. A chemist's view of the analysis of human hair for trace elements. Sci Total Environ. 1980;14(1):53-75.

Protecting Children from Lead Dust Exposure. Time for Change.

Fri, 19 Jan 2018 09:42:00 -0800

Lead is an incredibly dangerous heavy metal with no known beneficial use in the body. It mimics calcium, affecting all calcium-dependent biological processes, and is known to disturb the cardiovascular, renal, endocrine, and nervous systems. In children, the brain is the most sensitive target, as the blood brain barrier is less effective in children than in adults, potentially causing developmental delays even at low levels of exposure [1].

Where Does the Lead in Dust Come From?

Dust lead concentrations are significantly elevated in areas where there was heavy motor vehicle traffic during the time when leaded gasoline was still in use, and around buildings coated with lead-based paint before it was banned.

How Does Lead Dust Affect Children?

Children are more susceptible than adults to lead exposure due to increased contact with dust and dirt contaminated with lead, increased hand-to-mouth contact, and higher absorption of lead in the gastrointestinal tract. Lead from past sources of contamination is still present in some areas, and this is generally more of a problem for lower income families and minorities that live in older housing without lead remediation. It is estimated that interventions to reduce lead exposure since the 1970s have raised the mean IQ by as much as 4.5 points in the United States [2]. This is great news, but recent research has shown that even low levels of lead exposure can be damaging, especially for children. In 2012, the CDC (Centers for Disease Control and Prevention) stated that there is no safe level of lead exposure in children [3]. A recent study completed in Rhode Island found that in 71,000 children born between 1997 and 2005 a 1 µg/dL increase in blood lead levels was associated with a 3.1% reduction in 3^rd grade reading scores [4]. A 2009 study found that a return of $17-221 could be achieved for every $1 invested in lead paint hazard control, due to the costs of childhood lead exposure relating to public safety, productivity and health care [5].

Has Anything Been Done Recently to Protect Children from Lead Contamination in Dust?

The EPA itself acknowledged that "lead poisoning is the number one environmental health threat in the US for children ages 6 and younger."

Not really. The EPA (Environmental Protection Agency) set standards in 2001 for lead contamination in soil and dust. In 2011 it was widely agreed that there needed to be stricter standards, but no timelines were set. Fast forward 6 years to 2017, and the EPA requested another 6 years to implement new regulations. On December 27, 2017, the US Circuit Court of Appeals for the Ninth Circuit in San Francisco ruled 2-1 that the EPA had 90 days to propose a new rule and implement it within a year, and at this point it is unclear if the EPA will appeal the ruling or update regulations. The EPA itself acknowledged that "lead poisoning is the number one environmental health threat in the US for children ages 6 and younger."

Sensitive Lead Testing to Monitor Exposure is Necessary

The most commonly accepted way to measure exposure to lead is by testing venous or capillary whole blood. Many laboratories and doctors’ offices have outdated testing methods that once catered to the high blood lead levels of the past (≥10 µg/dL). The CDC showed that 40% of laboratories participating in the LAMP (Lead and Multi-Element Proficiency) quality assurance program couldn’t detect a target blood level of 1.48 µg/dL, and through 2015 only 22% of laboratories reported a limit of detection <1 µg/dL [6]. This is a problem, as 94.9% of over 5 million children tested between 2009 and 2015 had lead results <3 µg/dL [7]. One of the most popular lead testing devices, the Lead Care II analyzer, has a lower range limit of 3.3 µg/dL, which is not sensitive enough to differentiate levels of blood lead that are now considered dangerous [8]. ZRT Laboratory uses gold standard ICP-DRC-MS (inductively coupled dynamic reaction cell mass spectrometry) to test capillary blood spot lead levels, with a 0.2 µg/dL limit of detection, capable of measuring lead levels across multiple orders of magnitude.

Time for Change

It is time that the EPA takes action to prevent unnecessary exposure to lead. Past lead reduction programs have been very successful in reducing blood lead levels and helping prevent biological damage. It is also crucial that parents help to protect children by participating in blood, water, and dust lead screening programs, many which are available free of cost. It is now widely accepted that there is no safe level of exposure, and that delaying regulatory changes will undoubtedly result in unnecessary harm for both children and adults

More about Elements Testing

References

[1] Lidsky TI, Schneider JS. Lead neurotoxicity in children: basic mechanisms and clinical correlates. Brain. 2003;126(Pt 1):5-19.

[2] Kaufman AS, Zhou X, Reynolds MR, Kaufman NL, Green GP, Weiss LG. The possible societal impact of the decrease in U.S. blood lead levels on adult IQ. Environ Res. 2014;132:413-20.

[3] CDC (2012), Low Level Lead Exposure Harms Children: A Renewed Call for Primary Prevention: Report to the CDCP by the Advisory Committee on Childhood Lead Poisoning Prevention of the U.S. Centers for Disease Control: Atlanta, GA, USA, The Centers for Disease Control (US).

[4] Aizer A, Currie J, Simon P, Vivier P. Do Low Levels of Blood Lead Reduce Children's Future Test Scores? American Economic Journal: Applied Economics. 2018; 10:307-345.

[5] Gould E1. Childhood lead poisoning: conservative estimates of the social and economic benefits of lead hazard control. Environ Health Perspect. 2009;117:1162-7..

[6] Caldwell KL, Cheng PY, Jarrett JM, Makhmudov A, Vance K, Ward CD, Jones RL, Mortensen ME. Measurement Challenges at Low Blood Lead Levels. Pediatrics. 2017;140(2).

[7] McClure LF, Niles JK, Kaufman HW. Blood Lead Levels in Young Children: US, 2009-2015. J Pediatr. 2016;175:173-81..

[8] http://www.leadcare2.com/Product-Support/Product-Specifications

Toxic Baby Food: A Look Beyond the Labels

Fri, 27 Oct 2017 11:44:00 -0700

A recent news story [1] reports that the Clean Label Project, a non-profit organization focused on health and transparency in consumer product labeling, tested 530 baby food products for toxic elements and chemicals. The results were not good.

Sixty-five percent of products tested "positive" for arsenic, 36% for lead, 58% for cadmium, and the tests even showed high levels of BPA in “BPA Free” products. These toxins are harmful to infants (and adults), and can lead to developmental delays and permanent damage to the brain, kidneys, liver, bladder, and many other organs in the body. Arsenic and cadmium are known carcinogens while lead, a damaging neurotoxin, accumulates in bone and is released back into the bloodstream when bones develop (a continuous source of exposure) [2].

All toxin exposure should be limited, especially during infancy and childhood when the brain and other organ development is at its most sensitive.

Reviewing the "Proof"

It's important to know whether the amounts this project found in baby food are at a level higher than expected or at levels that are hazardous when ingested.

The first thing I do when I read an article like this is look for proof. What are their testing methods? How did they analyze the samples? Did they look at total levels of toxins, or speciate the samples? Is the work peer reviewed? Do the authors have something to gain from the study?

In this project, the samples were tested by a third-party laboratory. Their element testing was done by Inductively Coupled Plasma Mass Spectrometry (ICP-MS), which is what we use for element testing at ZRT Laboratory. However, their detection limits are very high in comparison to ours, which brings up the question as to how sensitive their testing is.

No one wants to have metals in their foods, but the reality is that trace amounts of metals are found in lots of foods. It is therefore important to know whether the amounts that this project found in the baby food are at a level higher than expected or at levels that have been found to be hazardous when ingested.

Unfortunately, the project isn’t sharing this information. This study is also not published by a peer-reviewed journal where the authors would be expected to answer these questions.

ICP-MS Element Detection Limits
	Clean Label Project (Food)	ZRT Laboratory (Urine/Blood)
Lead	4 ppb*	0.02 ppb
Arsenic	4 ppb	0.3 ppb
Mercury	2 ppb	0.05 ppb
Cadmium	2 ppb	0.08 ppb

*ppb = Parts per Billion

Practical Ways to Cope with Toxin Exposure

We are exposed to toxins every day. For the most part it is unavoidable, but making smart lifestyle choices for yourself or your loved ones can help reduce exposure.

The only true way to tell if you are currently being exposed to toxins, or have been exposed to them in the past, is to test for their presence in blood and/or urine.

Making sure the water you drink is free of contaminants and understanding where toxins come from is most important, as it helps you avoid products that can be dangerous. For example, rice takes up arsenic and cadmium from the water in paddy fields, so limiting consumption of rice products will reduce exposure to these toxins [3]. Choosing products that are routinely tested for toxins is smart, too, but these options are not always available – which is the Clean Label Project’s entire mission.

The only true way to tell if you are currently being exposed to toxins, or have been exposed to them in the past, is to test for their presence in blood and/or urine. There is no way to test all the foods we eat, or eliminate exposure from toxins completely. One batch of food may be completely different from the next, or the source of the food may change. Even the time of the year can affect toxin concentration.

ZRT offers a blood spot element test, which is ideal for looking at toxins like lead and organic mercury. We also offer a dried urine element test that provides the best assessment of total arsenic, cadmium, and inorganic mercury. We also test essential elements like selenium and zinc, which are known to help prevent or reduce the toxicity as a result of heavy metal exposure.

Learn more about why sample type matters when testing elements.

Don't Jump to Conclusons without Facts

Independent reviews like the one on baby food by the Clean Label Project can be helpful in making smart food choices, but it is important to separate good science from bad. In this case, without knowing who did the testing, what the test results were, or how food products were rated, I would recommend caution in drawing any firm conclusions.

More about Elements Testing

References

[1] https://www.usatoday.com/story/news/nation-now/2017/10/25/these-baby-foods-and-formulas-tested-positive-arsenic-lead-and-bpa-new-study/794291001/

[2] https://www.cancer.org/cancer/cancer-causes/general-info/known-and-probable-human-carcinogens.html

[3] /blog/archive/arsenic-exposure-from-rice-and-rice-based-breakfast-cereals

Does Following a Gluten-Free, Vegetarian or Vegan Diet Result in Increased Heavy Metals Intake?

Fri, 17 Mar 2017 10:40:00 -0700

A recent study from researchers at the Mayo Clinic in conjunction with the Centers for Disease Control and Prevention (CDC) revealed that people following a gluten-free diet have significantly higher arsenic, cadmium, lead, and mercury levels in urine and blood than those not following a gluten-free diet. [1]

Another similar study in 2006 revealed that vegans and vegetarians have an increased cadmium body burden in comparison to those following normal diets. [2]

So why do gluten-free, vegetarian, and vegan diets increase the risk of heavy metal exposure? Increased consumption of two foods that are staples for all cultures around the world are the primary culprits: rice and green leafy vegetables.

Why Rice & Green Leafy Vegetables?

Rice is by far the most commonly consumed food in the world. It can be made into numerous products such as bread, crackers, cereals, pastas, and beverages using processed rice flour and starch. Rice is normally grown in flooded fields so that competing plants are drowned out, but the water and soil may be contaminated with heavy metals from industrial pollutants and/or fertilizers. Well water used for irrigation can also contain naturally high levels of heavy metals such as arsenic that are readily absorbed by the plant. Rice paddies are an ideal environment for sulfur-reducing bacteria that are capable of converting less toxic inorganic mercury into very toxic organic mercury. People strictly following a gluten-free diet are primarily consuming rice and rice-based products due to its substitution into products in place of wheat, oat, rye, and barley, increasing their chance of exposure to heavy metals such as arsenic, cadmium, lead, and mercury.

Green leafy vegetables are also potentially a heavy metal source for those with high vegetable intake. Cadmium present in soil from pollution or natural sources is efficiently taken up by green leafy plants. Although absorption of cadmium in the gut is low, its half-life of over 20 years in the body results in steady buildup over time. A study revealed that blood cadmium levels were around 6x higher in vegans and 3x higher in vegetarians due to increased vegetable consumption in comparison to those eating a standard diet. [2] Interestingly enough, a population study showed that women with a postsecondary education who consume a diet high in vegetables and whole grains were exposed to higher amounts of cadmium. [3]

What is the Food and Drug Administration Doing?

It is impossible to know the level of heavy metals in food without laboratory testing, but making smart food choices can help reduce the risk of exposure.

The Food and Drug Administration (FDA) oversees food imports from foreign countries along with food from domestic sources, but tests less than one percent of imported food, primarily for food borne pathogens and spoilage. International importers must register with the FDA, comply with regulations, and allow inspections in order to import food into the United States. A very small percentage of domestic and imported non-seafoods are tested for lead, but not other heavy metals like cadmium, arsenic, and mercury. There are currently no requirements to list heavy metal concentrations on food labels.

How to Select Safe Foods and Prevent Excessive Heavy Metal Exposure

It is impossible to know the level of heavy metals in food without laboratory testing, but making smart food choices can help reduce the risk of exposure. Consumer Reports released information on which brands of rice had the highest arsenic content and helped explain the differences between the many variations. Certain types of rice, such as white rice, contain lower concentrations of heavy metals due to the stripping of both nutrients and toxins during the milling process. Selenium is an essential nutrient that binds tightly with arsenic and mercury and help to prevents oxidative damage, so it is important to consume an adequate amount.

A couple of ways to reduce cadmium exposure are to make sure your diet has adequate zinc (competing element) and to avoid foods known to be high in cadmium. According to the FDA, the foods highest in cadmium are spinach, lettuce, potatoes, sunflower seeds and strawberries. If you eat out of a garden at home, consider testing your soil and water for heavy metals. Eating a well-balanced, varied diet can also help prevent excessive exposure from a single source.

Testing for Heavy Metals

It's relatively easy to find out if you are unknowingly being exposed to heavy metals, whether it is from food, environmental, or occupational exposure. ZRT Laboratory has developed dried urine and dried blood spot assays that measure arsenic, cadmium, lead, and mercury along with essential elements using the most suitable sample types for each element. Urine and blood samples can easily be collected at home and sent directly to ZRT Laboratory for analysis. Checking both blood and urine levels for heavy metals will help determine short and long term exposure to heavy metals, especially if a restricted diet is followed.

More about Elements Testing

References

[1] Raehsler SL, Choung RS, Marietta EV, Murray JA. Accumulation of Heavy Metals in People on a Gluten-Free Diet. Clin Gastroenterol Hepatol. 2017 Feb 18.

[2] Krajcovicová-Kudládková M, Ursínyová M, Masánová V, Béderová A, Valachovicová M. Cadmium blood concentrations in relation to nutrition. Cent Eur J Public Health. 2006 Sep;14(3):126-9.

[3] Akesson A, Julin B, Wolk A. Long-term dietary cadmium intake and postmenopausal endometrial cancer incidence: a population-based prospective cohort study. Cancer Res. 2008 Aug 1;68(15):6435-41.

Lax Demolition Laws Lead to Toxic Neighborhoods. Goodbye Old House, Hello Lead Dust!

Wed, 09 Nov 2016 12:50:00 -0800

Over the past year there has been a plethora of news stories about lead exposure. From Flint, Michigan to Portland, Oregon, details have emerged about schools, homes, water supplies, and other areas and structures contaminated by lead. It hardly surprises me when these pop up in the news, as lead has been used generously in piping, paint, gasoline, ammunition, and batteries, among many other products during the last century.

A recent story about demolition of old buildings and houses leading to lead exposure caught my attention, as I had never considered this as a source of exposure even after years of researching lead. [1] The number of demolitions in the Pacific Northwest has shot up rapidly, and with it, concerns from neighbors about lead dust exposure and lax demolition regulations.

The Source of the Problem - Lead in Paint

Lead was added to paint up until 1977 when it was eventually banned because children were being poisoned from consumption of paint chips. Lead’s ability to increase paint durability, resist moisture, speed up drying, and retain a “new” look were the primary reasons for its addition to paint. In the early 1900s up to 70% of the pigments contained in paint were lead-based, with a single paint can weighing nearly 15 pounds. This resulted in hundreds of pounds of lead being painted in multiple coats across walls, windowsills, and other parts of homes built before 1978. This has become a major problem for most cities in the United States, as a vast majority of houses built prior to 1978 are coated in lead and are deteriorating.

Precautions to Reduce Lead Dust during Demolitions

New research is revealing the dangers of lead exposure at levels far lower than was once thought safe, especially for children.

The current demolition regulations have a lead “loophole” in which there is no requirement to trap lead dust. Remodel and repair jobs, on the other hand, have strict regulations that require safety precautions to be taken to prevent spreading of lead dust and paint debris. Some companies have taken it upon themselves to prevent neighborhood lead exposure during demolition by removing doors, windows, and railings coated in lead paint prior to demolition, and/or by applying water to knock down dust, demolishing on a rainy day, or working during times where there is little wind. It has been shown that lead dust from demolition can travel up to 400ft if the conditions are right. [2] Lead dust can deposit on surrounding soil, homes, sidewalks, and playgrounds, resulting in inhalation by humans, especially on hot and dry summer days. [3] [4]

In many cases, soil around demolition sites becomes unsafe due to lead contamination and has to be replaced with new topsoil. [5] Lead dust can be tracked inside houses where it deposits on the floor and remains a serious health risk for toddlers and animals. [6] Studies have shown increased blood lead levels in children that live around demolition activity, including one completed in New York that linked 14% of all elevated blood lead levels in children to demolition and renovation projects. [7] [8] [9]

Help is on the Way

Lead is a bio-accumulating neurotoxin, with no safe exposure level. New research is revealing the dangers of lead exposure at levels far lower than was once thought safe, especially for children. Lawmakers are currently working to fix the lead demolition “loophole,” which will hopefully create new regulations and restrictions for home demolitions to protect humans and animals. Precautionary steps can be taken to prevent lead dust exposure, such as leaving shoes at the door, washing hands, wiping down surfaces with a wet towel or mop, and preventing unnecessary contact with soil. [10]

If you are concerned about whether or not you or your family has been exposed to lead, ZRT Laboratory offers a simple at-home finger prick blood spot test that accurately measures lead, along with mercury, cadmium, selenium, zinc, copper and magnesium. For extra information on childhood lead exposure, please read our recent blogs on how blood lead results can be misleading and 10 need-to-know facts about lead.

More about Elements Testing

References

[1] http://www.portlandmercury.com/news/2016/09/28/18593355/no-ones-policing-lead-dust-in-demolition-happy-portland?mc_cid=51c23aed36&mc_eid=344742dd5c

[2] Jacobs DE, Cali S, Welch A, Catalin B, Dixon SL, Evens A, Mucha AP, Vahl N, Erdal S, Bartlett J. Lead and other heavy metals in dust fall from single-family housing demolition. Public Health Rep. 2013 Nov-Dec;128(6):454-62.

[3] Lanphear BP, Roghmann KJ. Pathways of lead exposure in urban children. Environ Res. 1997;74(1):67-73.

[4] Laidlaw MA, Filippelli GM, Sadler RC, Gonzales CR, Ball AS, Mielke HW. Children's Blood Lead Seasonality in Flint, Michigan (USA), and Soil-Sourced Lead Hazard Risks. Int J Environ Res Public Health. 2016 Mar 25;13(4):358. doi: 10.3390/ijerph13040358.

[5] Clark S, Menrath W, Chen M, Succop P, Bornschein R, Galke W, Wilson J. The influence of exterior dust and soil lead on interior dust lead levels in housing that had undergone lead-based paint hazard control. J Occup Environ Hyg. 2004 May;1(5):273-82.

[6] Caravanos J, Weiss AL, Blaise MJ, Jaeger RJ. A survey of spatially distributed exterior dust lead loadings in New York City. Environ Res. 2006 Feb;100(2):165-72. Epub 2005 Jul 11.

[7] Farfel MR, Orlova AO, Lees PS, Rohde C, Ashley PJ, Chisolm JJ Jr. A study of urban housing demolitions as sources of lead in ambient dust: demolition practices and exterior dust fall. Environ Health Perspect. 2003 Jul;111(9):1228-34.

[8] Rabito FA, Iqbal S, Shorter CF, Osman P, Philips PE, Langlois E, White LE. The association between demolition activity and children's blood lead levels. Environ Res. 2007 Mar;103(3):345-51. Epub 2006 Nov 30.

[9] CDC (Centers for Disease Control and Prevention) 2009. Children with elevated blood lead levels related to home renovation, repair, and painting activities—New York State, 2006–2007. MMWR Morb Mortal Wkly Rep 58(3):55–58.

[10] http://www.cdc.gov/nceh/lead/tips.htm

Testing "Low" For Lead - Why Your Child's Results May Be Misleading

Wed, 22 Jun 2016 11:24:00 -0700

The lead exposure stories that have dominated U.S. news recently now have parents scrambling to determine if their children have been exposed.

Parents are right to be worried because lead affects children differently than adults, primarily due to its detrimental effects on a developing brain and nervous system. I covered 10 need-to-know facts about childhood lead poisoning in an earlier blog.

In most cases if lead is detected in a school or community, free lead screening events for young children (1-5 years old) are made available. Parents should definitely take advantage of these programs, but they should look closely at the results they're getting.

Caveat to LeadCare II Blood Screening

Nearly all free testing events use a CLIA-waived on-the-spot LeadCare II screening device. The process is to prick the finger and collect two drops of capillary blood for a rapid 3-minute analysis. Even though I support free lead testing for young children, there is a certain caveat with LeadCare II analysis that is worth mentioning: the minimum reportable value.

The minimum reportable value of the LeadCare II system is 3.3 µg/dL, most likely due to method constraints.[1] [2] If a result falls below 3.3 µg/dL then the analyzer display reads "low" and the result is reported as less than 3.3 µg/dL. The current blood lead level of concern in children is 5 µg/dL; it was 60 µg/dL in 1970, 30 µg/dL in 1985, 25 µg/dL in 1991, and 10 µg/dL in 2012.[3] The trend here is obvious, highlighting how our understanding of low level lead exposure and the damage it causes to a developing brain and nervous system has evolved over the years.

What's the problem with a minimum reportable blood lead value of 3.3 µg/dL?

For every 1 µg/dL increase in blood lead in children, there is on average a 1.37-point decrease in IQ (in the range of 0 to 10 µg/dL).

The Fourth National Report on Human Exposure to Environmental Chemicals (2011-2012) prepared by the Centers for Disease Control and Prevention (CDC) showed that the average blood lead level for 1 to 5 year olds in the United States was 0.97 µg/dL, while the top 5% of children had blood lead levels over 2.91 µg/dL.[4] Many children testing in the top 5% for blood lead levels in the United States would be considered "low" using the LeadCare II screening device cutoff of 3.3 µg/dL. Several large scale studies have shown that there is a greater loss of IQ points when blood lead levels increase from 0 to 10 µg/dL than when it raises over 10 µg/dL.[5] [6] For every 1 µg/dL increase in blood lead in children, there is on average a 1.37-point decrease in IQ (in the range of 0 to 10 µg/dL).[5]

Studies by Miranda et al.[7] and Evans et al.[8] show how detrimental low level lead exposure can be. Even a blood lead level increase from 1 µg/dL to 2 µg/dL in children is damaging. Remember, there is no safe level of lead exposure in children, according to the guidelines issued by the CDC in 2012.

How do you determine blood lead less than 3.3 µg/dL?

The CDC, along with ZRT Laboratory, uses inductively coupled plasma mass spectrometry (ICP-MS) which is the gold standard for element analysis. Our blood spot lead assay, which can be completed at home, can accurately detect down to 0.22 µg/dL, and provides quantitative results that can be compared to those of a reference population and published childhood health guidelines. Other instrumentation can measure low blood lead levels, but do not match the sensitivity and specificity of ICP-MS.

In Conclusion

Free lead testing using the LeadCare II screening device may be useful as a quick check to rule out very high exposure, but in order to quantitatively determine the extent of a child’s exposure, more sophisticated and sensitive testing is required.

More about Elements Testing

References

[1] http://www.lcultra.com/getmedia/7bed0248-3d0f-4ac0-8d51-235f75ba77e8/M-0029-Rev-01-LCUltra-vs-Reference-Method.pdf.aspx

[2] http://www.leadcare2.com/getmedia/73ac501b-35e3-4d74-b6a9-9e7fc51adef0/70-6551_Rev_07_User-s_Guide,_LeadCare_II_(PRINT)-1.pdf.aspx

[3] http://www.atsdr.cdc.gov/csem/csem.asp?csem=7&po=8

[4] Centers for Disease Control and Prevention. Fourth Report on Human Exposure to Environmental Chemicals, Updated Tables, (February, 2015). Atlanta, GA: U.S. Department of Health and Human Services, Centers for Disease Control and Prevention. http://www.cdc.gov/exposurereport/

[5] Canfield RL, Henderson CR, Cory-Slechta DA, Cox C, Jusko TA, Lanphear BP. Intellectual impairment in children with blood lead concentrations below 10 μg per deciliter. N Eng J Med. 2003;348:1517–26.

[6] Lanphear BP, Hornung R, Khoury J, Yolton K, Baghurst P, Bellinger DC, Canfield RL, Dietrich KN, Bornschein R, Greene T, Rothenberg SJ, Needleman HL, Schnaas L, Wasserman G, Graziano J, Roberts R. Low-level environmental lead exposure and children's intellectual function: an international pooled analysis. Environ Health Perspect. 2005 Jul;113(7):894-9.

[7] Miranda ML, Kim D, Galeano MA, Paul CJ, Hull AP, Morgan SP. The relationship between early childhood blood lead levels and performance on end-of-grade tests. Environ Health Perspect. 2007 Aug;115(8):1242-7.
http://europepmc.org/articles/PMC1940087

[8] Evens A, Hryhorczuk D, Lanphear BP, Rankin KM, Lewis DA, Forst L, Rosenberg D. The impact of low-level lead toxicity on school performance among children in the Chicago Public Schools: a population-based retrospective cohort study. Environ Health. 2015 Apr 7;14:21. http://ehjournal.biomedcentral.com/articles/10.1186/s12940-015-0008-9

Lead Poisoning - Is Your Child at Risk? (Plus 10 Need-to-Know Facts)

Tue, 07 Jun 2016 09:26:00 -0700

Over the past few months there has been a spike in news stories related to elevated lead levels in U.S. public water systems, beginning with the crisis in Flint, Michigan. This has initiated investigations into current water testing methods and probes into violations that have been swept under the rug.

In many cases the public water supply is safe, but there's a hidden concern you need to know about – the immediate plumbing leading to drinking fountains, faucets, bathrooms, etc. in houses, apartments, schools, and workplaces could be leaching lead into the water. This can be caused by changes in water pH and temperature, additives, or the age and condition of pipes and connections.

Even though leaded gasoline, paint, and plumbing were phased out in the 1970s, they also will remain sources of lead exposure far into the future.

Children are Most at Risk

Adults absorb around 15% of lead they ingest, while children and pregnant women absorb around 50%.

Recently, water testing in the Pacific Northwest revealed elevated levels of lead in public schools. Most schools built decades ago have ancient plumbing systems that are slowly poisoning those most susceptible to lead – CHILDREN.

This is not a localized problem, but a well understood and dangerous one across the U.S. and throughout the world. As individuals become more educated on the dangers of lead and sources of exposure, we can expect more stories to break that uncover hidden sources of lead and other toxic metals such as mercury, cadmium, and arsenic. Remember, the CDC has stated that there is no safe level of lead exposure for children.[1]

10 Need-to-Know Facts on Childhood Lead Exposure

Childhood lead exposure is estimated to cause the US $61 billion in economic losses due to lead's neurotoxic effects leading to a decreased intelligence quotient (IQ).[2]
Young children aged 1-5 years had average blood levels of 15 µg/dL in the 1970s, which dropped to 1.9 µg/dL in 1999, largely due to the ban on lead in gas, plumbing, and paint.[3] A blood lead level of 5 µg/dL is considered to be toxic for children.[4] Recent studies have shown that behavioral and neurological effects can occur at blood lead levels below 5 µg/dL.[5]
In 2012, approximately 450,000 children in the US had blood lead levels above 5 µg/dL.[6]
Adults absorb around 15% of lead they ingest while children and pregnant women absorb around 50%.[7]
Blood transfusions can be a significant source of lead exposure in infants and young children.[8]
Children with elevated blood lead levels may show little or no symptoms. Some of the symptoms associated with childhood lead exposure are: headache, lack of appetite, constipation, agitation, clumsiness, sleepiness, stomach pain, agitation, anemia, learning disabilities, and kidney failure.[9]
Lead in dust and dirt is a major source of exposure for young children that are learning to crawl or walk, as it is easily consumed or inhaled.[10]
Bone is the major target organ for lead, and because of continual bone remodeling during growth in children, lead is constantly being reintroduced into the bloodstream.[11]
Lead affects the development of a child’s brain and nervous system, putting them at greater risk than adults.[12]
Blood lead levels peak during dry, warmer periods of the year.[13] This is due to inhalation and ingestion of lead in dust originating primarily from prior use in gasoline.

Preventing & Detecting Lead Exposure

The half-life of lead in blood is 35 days, so it is important to test as soon as possible if you believe exposure has occurred.

The best way to prevent lead exposure in children is to remove them from the source. Do you know if your house has lead pipes or paint? Has your school’s water been tested recently and will they provide the method of sampling and results?
Make sure that your child washes his or her hands prior to eating or after playing in dirt, as absorption of lead by ingestion is much higher in children than adults.
If you have a vegetable garden or grow fruit trees, get your soil tested for heavy metals. Plants are efficient at sucking up toxins from the soil, especially metals, which will give you a good dose if eaten.
Inside air is often much more toxic than outdoor air, because we track toxins into our home and then they stay there, getting more concentrated over time. Leave your shoes by the door so you don’t bring pollutants into your living space.
Proper nutrition is important in reducing intestinal uptake and the damaging effects of lead. Dietary zinc and selenium have been shown to decrease absorption of, and form complexes with, lead, reducing its availability.[14] [15] Is your child consuming a healthy, nutritious diet with adequate levels of essential nutrients such as zinc, selenium, iron, and calcium?

The Take-Away

Lead is a dangerous neurotoxin and a probable human carcinogen that is most detrimental to the developing brain and nervous system of a child. It is essential to detect exposure to lead and other toxic metals as soon as possible, as there is very little that can reverse the effects of long term heavy metal exposure.

Testing blood lead levels is the most accurate and common way to determine recent and past exposure in a child. The half-life of lead in blood is 35 days, so it is important to test as soon as possible if you believe exposure has occurred.[16] Once lead enters bone, its half-life is up to 30 years.

Talk to your doctor about testing, and make sure to ask if he or she is testing lead in whole blood. Testing serum or urine is not ideal, as almost all lead is attached to hemoglobin in red blood cells.

If you're worried about needles, consider a simple finger-prick blood test that can be completed at home as an effective and less stressful alternative, especially for children.

More About Heavy Metals Element Testing

References

[1] Schnur J, John RM. Childhood lead poisoning and the new Centers for Disease Control and Prevention guidelines for lead exposure. J Am Assoc Nurse Pract. 2014;26:238-47

[2] Trasande L, Liu Y. Reducing the staggering costs of environmental disease in children, estimated at $76.6 billion in 2008. Health Aff (Millwood). 2011 May;30(5):863-70.

[3] Gorospe EC, Gerstenberger SL. Atypical sources of childhood lead poisoning in the United States: a systematic review from 1966-2006. Clin Toxicol (Phila). 2008 Sep;46(8):728-37.

[4] CDC. Advisory Committee on Childhood Lead Poisoning Prevention. Low level lead exposure harms children: a renewed call for primary prevention. CDC. Available at: http://www.cdc.gov/nceh/lead/acclpp/final_document_030712.pdf.

[5] Health Canada. Second Report on Human Biomonitoring of Environmental Chemicals in Canada; Health Canada: Ottawa, ON, Canada, 2013.

[6] "CDC Response to Advisory Committee on Childhood Lead Poisoning Prevention" (PDF). http://www.cdc.gov/nceh/lead/acclpp/cdc_response_lead_exposure_recs.pdf.

[7] Wigle DT. Child Health and the Environment. New York, NY: Oxford University Press; 2003.

[8] Gehrie E, Keiser A, Dawling S, Travis J, Strathmann FG, Booth GS. Primary prevention of pediatric lead exposure requires new approaches to transfusion screening. J Pediatr. 2013 Sep;163(3):855-9.

[9] American Academy of Pediatrics, Committee on Environmental Health. Lead Exposure in Children: Prevention, Detection, and Management. Policy Statement. Pediatrics. 2005; 116: 1036-1046. Affirmed Jan 2009.

[10] Woolf AD, Goldman R, Bellinger DC. Update on the clinical management of childhood lead poisoning. Pediatr Clin North Am. 2007 Apr;54(2):271-94, viii.

[11] Barbosa F Jr, Tanus-Santos JE, Gerlach RF, Parsons PJ. A critical review of biomarkers used for monitoring human exposure to lead: advantages, limitations, and future needs. Environ Health Perspect. 2005 Dec;113(12):1669-74.

[12] Sanders T, Liu Y, Buchner V, Tchounwou PB. Neurotoxic effects and biomarkers of lead exposure: a review. Rev Environ Health. 2009 Jan-Mar;24(1):15-45.

[13] Centers for Disease Control and Prevention (CDC). Morbidity and Mortality Weekly Report (MMWR) Childhood Blood Lead Levels—United States, 2007–2012. Available online: http://www.cdc.gov/mmwr/preview/mmwrhtml/mm6254a5.htm?s_cid=mm6254a5_x.

[14] Ahamed M, Singh S, Behari JR, Kumar A, Siddiqui MK. Interaction of lead with some essential trace metals in the blood of anemic children from Lucknow, India. Clin Chim Acta. 2007 Feb;377(1-2):92-7.

[15] Kargacin, B., Kostial, K., 1991. Toxic metals: In fluence of macromolecular dietary components on metabolism and toxicity. In: Rowland, I.R. (Ed.), Nutrition, toxicity, and cancer. CRC Press, Boca Raton, pp. 197–221.

[16] Papanikolaou NC, Hatzidaki EG, Belivanis S, Tzanakakis GN, Tsatsakis AM. Lead toxicity update. A brief review. Med Sci Monit. 2005 Oct;11(10):RA329-36.

Elements Testing – Why Sample Type Matters!

Tue, 03 May 2016 10:24:00 -0700

Urine, serum, plasma, whole blood, red blood cells, feces, hair, fingernails…the list goes on.

How do you decide what biological sample(s) to use for element analysis? Can results be compared to scientific literature or do they have clinical significance? Is it possible for values to be elevated or low in one sample type and normal in another? Do test results indicate recent intake, body burden, acute toxicity, chronic toxicity, deficiency, or homeostatic regulation?

These are just some of the questions facing a testing laboratory when they want to develop and validate essential and toxic element profiles that will provide clinically meaningful results.

Most element panels commercially available today consist of 20-30 elements analyzed using a single sample type (most commonly urine or serum). It may seem like a reasonable one-stop-shop for element analysis, but this is not the case!

Each element is unique in the way it is excreted, when it is excreted, and how results should be interpreted. The problem with testing a single sample type is that results may be meaningful for one element, and meaningless for another. ZRT Laboratory prides itself in producing results with meaning, so instead of creating large element panels using a single sample type, we broke our element profiles up to test key toxic and essential elements in what we believe is the most clinically significant sample type.

This blog post focuses on key differences in element testing in urine, serum, and whole blood. Hair and nail analyses will not be discussed other than to say while they may have clinical utility, they are prone to contamination from external sources such as nail polish, cosmetics, personal hygiene products, or shampoo, introducing many more variables.

What we test and in which sample type

Urine (Dried Urine) – Iodine, Bromine, Selenium, Arsenic, Cadmium, and Mercury (plus Creatinine to correct for urine dilution)

Whole Blood (Blood Spot) – Zinc, Copper, Zinc/Copper Ratio, Magnesium, Selenium, Cadmium, Lead, and Mercury

Taking each element in turn, here's the rationale for the choice of sample type.

Iodine – Urine is the best indicator of recent dietary iodine intake, as >90% is excreted in urine.[1] Nearly all iodine related studies published by major health organizations and independent research groups have used urine iodine to determine deficiency and excess in populations and recent intake in individuals. Serum iodine is sometimes used in hospitals as a quick screen to detect acute exposure, but this is not common.

Bromine – Urine is the best indicator of recent dietary bromine intake, as the majority is excreted in urine.[2]

Selenium – Urine is the best indicator of recent dietary selenium intake, as 50-70% is excreted in urine.[3] Both whole blood and serum indicate current body selenium status, but whole blood is believed to reflect long term intake better than serum.[4] [5] The concentration of selenium in serum is about 80% of what you find in whole blood.[6]

Arsenic – Urinary arsenic is the best indicator of recent dietary intake, as 80% is excreted in urine after 3 days.[7] Serum and whole blood are poor indicators of recent dietary intake or body status for arsenic as it is cleared rapidly within a couple of hours.[8] Serum and blood should only be used to detect very recent or extremely high levels of exposure.[9]

Cadmium – Urinary cadmium is the best indicator of long term exposure to this toxic element. Cadmium is concentrated in the kidneys and urinary levels represent cumulative cadmium exposure over the long term (it has a 30 year half-life).[10] Whole blood cadmium levels reflect recent exposure within the last 50 days.[11] [12] Only about 0.01-0.02% of the total body cadmium burden is excreted every day because it accumulates primarily in the kidneys.[13] Serum is a poor indicator of exposure because cadmium in the bloodstream binds to red blood cells, with erythrocyte concentrations 20 times higher than serum.[14]

Lead – Whole blood is the best indicator of lead status and the most commonly used sample for population and individual monitoring.[15] Around 95% of lead is bound to red blood cells with the rest complexed with intracellular proteins.[15] Lead in serum is only 1% of what is found in whole blood.[16] [17] Lead is excreted very slowly in urine, and is only of interest for long term occupational monitoring programs and chelation therapy.[18] [19]

Mercury – Urinary mercury is the best indicator of inorganic and elemental mercury exposure and kidney burden.[20] [21] Whole blood is the best indicator of organic (methyl or ethyl) mercury exposure with 70-95% bound to hemoglobin in red blood cells and a half-life of around 50 days.[22] [23] [24] Serum should not be used for mercury analysis.[25]

Zinc and Copper – Whole blood or serum can be used to assess zinc and copper. Zinc and copper are functional antagonists; therefore, the zinc/copper ratio should be determined, especially in cases where values of both border high and low normal ranges.[26] Urinary zinc levels reflect recent intake, but studies have not been able to correlate urinary zinc to tissue concentrations.[27] In normal people, less than 3% of copper intake is excreted in urine.[28] Whole blood copper levels correlate better to symptoms of copper toxicity than serum, while whole blood zinc levels may better reflect intracellular and long term zinc status than serum.[29] [30] [31]

Magnesium – There is no simple laboratory test to indicate total body Mg status in humans.[32] Less than 1% of body magnesium is found in blood, with approximately 0.3% in serum.[33] Urinary magnesium reflects recent dietary intake and intestinal absorption, but is not commonly measured.[34] Serum magnesium is commonly tested, but there is little correlation to total body magnesium or concentrations in specific tissues. Serum magnesium levels are kept under tight homeostatic control, and are usually normal even when there is a nutritional magnesium deficiency because serum levels are raised at the expense of intracellular stores.[35] Whole blood magnesium contains a high concentration of magnesium ions which are essential for many metabolic processes and better reflects long term body status.[36] [37]

Examples

A patient regularly eats mercury-contaminated fish. Testing would potentially show low urinary and serum mercury, while whole blood tests would be high for mercury. This is because a majority of the mercury in fish tissue is methylmercury which can only be detected in whole blood samples.
A patient continuously drinks water contaminated with arsenic from a well. Testing would potentially show low whole blood and serum arsenic and high urinary arsenic. This is because arsenic is cleared rapidly in blood but is excreted over multiple days in urine.
A patient ceased smoking cigarettes (high source of cadmium) 6 months ago, but was a habitual smoker for 20 years. Whole blood and serum would potentially show low cadmium levels while urine tests high for cadmium. This is because whole blood represents recent cadmium intake and serum is a poor indicator of cadmium burden, while urine indicates long term cadmium exposure.

As you can see, proper sample type matters when testing toxic and essential elements. In certain cases testing two sample types will provide a better picture of total exposure.

More about Element Testing

References

[1] Hays MT. Estimation of total body iodine content in normal young men. Thyroid. 2001;11:671-5.

[2] van Leeuwen FX, Sangster B. The toxicology of bromide ion. Crit Rev Toxicol. 1987;18:189-213.

[3] Sanz Alaejos M, Díaz Romero C. Urinary selenium concentrations. Clin Chem. 1993;39:2040-52.

[4] Thomson CD. Assessment of requirements for selenium and adequacy of selenium status: a review. Eur J Clin Nutr. 2004;58:391-402.

[5] Ashton K, Hooper L, Harvey LJ, et al. Methods of assessment of selenium status in humans: a systematic review. Am J Clin Nutr 2009; 89: 2025S–39S.

[6] Combs GF, Jr. Selenium in global food systems. Br J Nutr 2001; 85: 517–47.

[7] Van Hulle M, Zhang C, Schotte B, et al. Identification of some arsenic species in human urine and blood after ingestion of Chinese seaweed Laminaria. J Anal At Spectrom. 2004;19:58-64.

[8] Baselt RC. Disposition of Toxic Drugs and Chemicals in Man. 7th ed. Foster City, CA: Biomedical Publications; 2004.

[9] Mandal BK, Suzuki KT. Arsenic round the world: a review. Talanta. 2002;58:201-35.

[10] Nordberg GF, Jin T, Kong Q, et al. Biological monitoring of cadmium exposure and renal effects in a population group residing in a polluted area in China. Sci Total Environ. 1997;199:111-4.

[11] Lauwerys R, Roels H, Regniers M, et al. Significance of cadmium concentration in blood and in urine in workers exposed to cadmium. Environ Res. 1979;20:375-91.

[12] Järup L, Rogenfelt A, Elinder CG, et al. Biological half-time of cadmium in the blood of workers after cessation of exposure. Scand J Work Environ Health. 1983;9:327-31.

[13] ATSDR (2008) Toxicological profile for cadmium. Agency for Toxic Substances and Disease Registry, Atlanta, GA

[14] Friberg L, Piscator M, Nordberg GF, Kjellstrom T. Cadmium in the Environment. 2nd ed. Cleveland, OH: CRC Press; 1974.

[15] Baselt RC. Disposition of Toxic Drugs and Chemicals in Man. 7th ed. Foster City, CA: Biomedical Publications; 2004.

[16] Manton WI, Rothenberg SJ, Manalo M. The lead content of blood serum. Environ Res. 2001;86:263-73.

[17] Schütz A, Bergdahl IA, Ekholm A, Skerfving S. Measurement by ICP-MS of lead in plasma and whole blood of lead workers and controls. Occup Environ Med. 1996;53:736-40.

[18] Pearson H.A.; Schonfeld, D.J. (2003). "Lead". In Rudolph, C.D. Rudolph's Pediatrics (21st ed.). McGraw-Hill Professional. ISBN 0-8385-8285-0.

[19] Barbosa F Jr, Tanus-Santos JE, Gerlach RF, Parsons PJ. A critical review of biomarkers used for monitoring human exposure to lead: advantages, limitations, and future needs. Environ Health Perspect. 2005;113:1669-74.

[20] Clarkson TW, Magos L. The toxicology of mercury and its chemical compounds. Crit Rev Toxicol. 2006;36:609-62.

[21] Holmes P, James KA, Levy LS. Is low-level environmental mercury exposure of concern to human health? Sci Total Environ. 2009;408:171-82.

[22] Bakir F, Damluji SF, Amin-Zaki L, et al. Methylmercury poisoning in Iraq. Science. 1973;181:230-41.

[23] Hansen JC, Tarp U, Bohm J. Prenatal exposure to methyl mercury among Greenlandic polar Inuits. Arch Environ Health. 1990;45:355-8.

[24] Kershaw TG, Clarkson TW, Dhahir PH. The relationship between blood levels and dose of methylmercury in man. Arch Environ Health. 1980;35:28-36.

[25] NCCLS. Control of Preanalytical Variation in Trace Element Determinations; Approved Guideline - 2nd edition. NCCLS document C38-A2. NCCLS, Wayne, PA, 2001.

[26] Bjorklund G. The role of zinc and copper in autism spectrum disorders. Acta Neurobiol Exp (Wars). 2013;73:225-36.

[27] Lowe NM, Fekete K, Decsi T. Methods of assessment of zinc status in humans: a systematic review. Am J Clin Nutr. 2009;89:2040S-2051S

[28] Luza SC, Speisky HC. Liver copper storage and transport during development: implications for cytotoxicity. Am J Clin Nutr. 1996;63:812S-20S.

[29] Gunay N, Yildirim C, Karcioglu O, et al. A series of patients in the emergency department diagnosed with copper poisoning: recognition equals treatment. Tohoku J Exp Med. 2006;209:243-8.

[30] Stewart-Knox BJ, Simpson EE, Parr H, et al. Zinc status and taste acuity in older Europeans: the ZENITH study. Eur J Clin Nutr. 2005;59 Suppl 2:S31-6.

[31] Roohani N, Hurrell R, Kelishadi R, Schulin R. Zinc and its importance for human health: An integrative review. J Res Med Sci. 2013;18:144-57.

[32] Arnaud MJ. Update on the assessment of magnesium status. Br J Nutr. 2008;99 Suppl 3:S24-36.

[33] Elin RJ. Laboratory tests for the assessment of magnesium status in humans. Magnes Trace Elem. 1991-1992;10:172-81.

[34] Witkowski M, Hubert J, Mazur A. Methods of assessment of magnesium status in humans: a systematic review. Magnes Res. 2011;24:163–180.

[35] Gibson, RS. Principles of Nutritional Assessment, 2nd ed. New York, NY: Oxford University Press, 2005.

[36] Bock JL, Wenz B, Gupta RK. Changes in intracellular Mg adenosine triphosphate and ionized Mg2+ during blood storage: detection by 31P nuclear magnetic resonance spectroscopy. Blood. 1985;65:1526-30.

[37] Deuster PA, Trostmann UH, Bernier LL, Dolev E. Indirect vs direct measurement of magnesium and zinc in erythrocytes. Clin Chem. 1987;33:529-32.

High Air Levels of Arsenic & Cadmium May Be Linked to a Cancer Cluster in Portland, Oregon

Thu, 04 Feb 2016 17:16:00 -0800

Many residents were surprised to learn that high levels of arsenic and cadmium are being detected at an air monitoring station in Southeast Portland, Oregon according to the state Department of Environmental Quality (DEQ).

Watch the News: Dr. Zava comments on toxin exposure in SE Portland

The state began monitoring air quality after moss samples taken from the area last October were found to be high in arsenic and cadmium. The results, which were only made public in the past few days, show cadmium at 49 times the acceptable level and arsenic at 159 times the acceptable level for air.

Of key concern is that the testing location is in an area populated with businesses, schools, and parks. It is not clear yet how long exposure has occurred or whether it is caused by a nearby glass blowing facility. As of this week, the glass blowing facility decided to cease use of arsenic and cadmium.

Investigating an Unusual Cluster of Breast Cancer Cases

More shocking is that there is a cluster of breast cancer cases in the same area of Southeast Portland that were reported on in 2013. Arsenic and cadmium, along with other toxic metals are known to be damaging to the body and to increase risk for heart disease and cancer.

Cadmium exposure specifically has been linked to an increased risk of breast cancer. Currently epidemiologists are looking to see if there is a relationship between the recent increase in breast cancer cases and the high levels of arsenic and cadmium in the local area.

Watch the Webinar: Toxic Heavy Metals & Risks for Cancer

Cadmium itself has a half-life in the body of 7-16 years, meaning that it is eliminated very slowly and causes significant damage as it builds up. The only real way to tell how much cadmium, arsenic, or any other toxin YOU are being exposed to is to test yourself for these heavy metals using a bodily substance such as blood, urine, hair, saliva or feces.

Read the Article: Bio-Accumulation of Toxic Elements

Simple Testing Reveals Element Exposure

Usually one sample type is better than others for determining long- or short-term exposure.

For example, it is best to measure arsenic exposure in urine, as urine is the primary excretion route and it is cleared relatively quickly in comparison to other heavy metals.

For cadmium, however, urine is the best indicator of long-term exposure while blood is a better indicator of short-term exposure.

If you’re concerned about exposure to excessive levels of heavy metals like cadmium or arsenic, simple testing can be revealing. Tests, such as those offered by ZRT Laboratory, are an accurate and effective way to determine levels of elements such as iodine, selenium, bromine, arsenic, mercury, and cadmium.

Whatever lab you choose, make sure its scientists are using Inductively Coupled Plasma-Mass Spectrometry, or ICP-MS, which is the most sophisticated test method available for measuring heavy metals as well as essential elements.

References

http://www.kgw.com/news/local/high-levels-of-cadmium-arsenic-detected-in-se-portland/32360056

http://blogtown.portlandmercury.com/BlogtownPDX/archives/2016/02/03/arsenic-cadmium-levels-near-two-se-portland-schools-are-alarmingly-high-state-finds

http://www.bullseyeglass.com/news-releases.html

Does Bioaccumulation of Toxic Elements Lead to Large Problems?

Fri, 02 Oct 2015 04:00:00 -0700

Bioaccumulation is the concentration of toxic substances by an organism over an extended period of time. This occurs in all species, and is magnified progressively up the food chain.

Toxic elements we consume in liquids and foods, breathe in from the air, or absorb through our skin are retained in the body for different durations, depending on their chemical properties. The amount of time it takes for the body to eliminate half of a specific substance is called its half-life.

Toxic heavy metals such as cadmium, mercury, and lead can accumulate over a lifetime and have long half-lives in different organs and tissues.

Cadmium

Cadmium is a toxic heavy metal that enters the body mostly through food consumption and tobacco smoke, as certain plants concentrate this heavy metal. Average cadmium absorption from food per day is around 1 µg, but those who smoke one pack of cigarettes per day (made from tobacco leaves) will take in an additional 1 to 3 µg.[1] Although this amount may not seem like a lot, cadmium is slowly eliminated from the body with a blood half-life of 75-128 days and a body half-life of 7-16 years.[2] Cadmium will primarily affect the kidneys, but also damages the nervous and cardiovascular systems, liver, lungs, pancreas, bones, and reproductive organs.[3] High cadmium levels have been linked to cancers of the reproductive organs, including the breasts, prostate, and uterus.[4] [5] [6] Cadmium is believed to increase cancers of estrogen-sensitive tissues by acting as a metalloestrogen to activate estrogen-regulated genes.[7]

Mercury

Mercury is a well-known toxic heavy metal that is present in different forms including inorganic, organic, and elemental species. Inorganic mercury’s target organs are the gut and kidney, while elemental and organic mercury primarily accumulates in fatty tissue such as the brain.[8] The half-life of elemental and inorganic mercury in blood is 40–60 days, while the half-life of organic mercury in blood is about 70 days.[9] [10] [11] Organic and elemental mercury can penetrate the blood-brain barrier and enter the brain where the elimination half-life of the heavy metal may exceed several years.[12] Mercury’s toxicity is primarily through the creation of reactive oxygen species (ROS) which burn-down antioxidants such as glutathione, and react with selenium-containing enzymes involved in antioxidant actions (e.g., glutathione peroxidase) and thyroid hormone formation (thyroid deiodinases).[13]

Lead

Lead is a neurotoxin that was present in paint and pipes until the 1970s and gas until the 1990s. Many houses built prior to the 1970s still have leaded paint and pipes, increasing exposure via food, water, and air in the home environment. Target organs of lead toxicity are the urinary, skeletal, immune, gastrointestinal, reproductive, cardiovascular, and nervous systems.[14] The half-life of lead in blood is around 30 days, while in bones it is much longer at 20-30 years.[15] Rapid breakdown of bone that occurs in some women at menopause can release a high level of lead that accumulated for years. [16]

What can you do to determine current heavy metal exposure?

ZRT now offers dried urine testing for three of the most prevalent toxic heavy metals (cadmium, mercury, and arsenic) in combination with the essential elements iodine and selenium. Currently we are developing a similar test for lead and other elements using whole blood, the best biomarker of lead exposure. Cadmium, mercury, and lead are three of the top ten most hazardous substances according to the Agency for Toxic Substances and Disease Registry’s (ATSDR) Priority List of Hazardous Substances, and along with arsenic make up the top four most hazardous heavy metals.[17]

It is important to know if you have been bioaccumulating heavy metals, as this could help identify and eliminate their source and help curb current or future health problems associated with their bioaccumulation.

Related Resources:

References

[1] Lewis GP, Coughlin LL, Jusko WJ, Hartz S. Contribution of cigarette smoking to cadmium accumulation in man. Lancet. 1972;1(7745):291-2.

[2] Järup L, Rogenfelt A, Elinder CG, Nogawa K, Kjellström T. Biological half-time of cadmium in the blood of workers after cessation of exposure. Scand J Work Environ Health. 1983;9(4):327-31.

[3] Nordberg GF. Historical perspectives on cadmium toxicology. Toxicol Appl Pharmacol. 2009;238(3):192-200.

[4] McElroy JA, Shafer MM, Trentham-Dietz A, Hampton JM, Newcomb PA. Cadmium exposure and breast cancer risk. J Natl Cancer Inst. 2006;98(12):869-73.

[5] Zeng X, Jin T, Jiang X, Kong Q, Ye T, Nordberg GF. Effects on the prostate of environmental cadmium exposure--a cross-sectional population study in China. Biometals. 2004;17(5):559-65.

[6] Akesson A, Julin B, Wolk A. Long-term dietary cadmium intake and postmenopausal endometrial cancer incidence: a population-based prospective cohort study. Cancer Res. 2008;68(15):6435-41.

[7] Kortenkamp A. Are cadmium and other heavy metal compounds acting as endocrine disrupters? Met Ions Life Sci. 2011;8:305-17.

[8] Park JD, Zheng W. Human exposure and health effects of inorganic and elemental mercury. J Prev Med Public Health. 2012;45(6):344-52.

[9] US Centers for Disease Control and Prevention (CDC). Third national report on human exposure to environmental chemicals. Atlanta: CDC; 2005. Available: www.cdc.gov/exposurereport/3rd/default.htm (accessed 2015 Aug 28).

[10] Agency for Toxic Substances and Disease Registry (ATSDR). Toxological profile for mercury. Washington (DC): ATSDR, Public Health Service, US Department of Health and Human Services; 1999. Available: www.atsdr.cdc.gov/toxprofiles/tp46.html (accessed 2014 Aug 28).

[11] Clarkson TW, Magos L, Myers GJ. The toxicology of mercury - current exposures and clinical manifestations. N Engl J Med 2003;349:1731-7.

[12] Petering HG, Tipper LB. Pharmacology and toxicology of heavy metals: mercury. Pharmacol Ther 1976;1:131–151.

[13] Cuvin-Aralar ML, Furness RW. Mercury and selenium interaction: a review. Ecotoxicol Environ Saf. 1991;21(3):348-64.

[14] ATSDR. 2007. Toxicological profile for lead. Atlanta, GA: US Department of Health and Human Services, Public Health Service, Agency for Toxic Substances and Disease Registry. p. 582.

[15] WHO. Lead. Environmental Health Criteria, vol. 165. Geneva: World Health Organization, 1995.

[16] Potula V, Kaye W. The impact of menopause and lifestyle factors on blood and bone lead levels among female former smelter workers: the Bunker Hill Study. Am J Ind Med. 2006;49(3):143-52.

[17] Agency for Toxic Substances & Disease Registry. Priority List of Hazardous Substances. Available at: http://www.atsdr.cdc.gov/SPL/index.html.

Colorado Mine Spill Makes High Levels of Heavy Metals a Threat to Humans & Wildlife

Mon, 17 Aug 2015 12:56:00 -0700

On August 5, 2015 the Environmental Protection Agency (EPA) accidentally breached a tunnel holding liquid waste as part of the cleanup of the Gold King Mine in Colorado.

This breach resulted in the release of 3 million gallons of toxic waste into Colorado’s Animas River. The waste stained the river yellow and continued to travel downstream into the San Juan River. The Animas and San Juan Rivers are a source of drinking and irrigation water, are heavily used for recreation, and are home to a wide variety of wildlife.

Water samples were tested on August 5 at multiple locations around the spill and results were made public by the EPA (Table 1).¹ One of the test locations was Cement Creek Bridge in Silverton, Colorado, which crosses over Cement Creek, the location of the spill. Cement Creek travels a short distance before it merges with the Animas River. Seen below are the reported water sample values and maximum contaminant levels (MCL) for arsenic, cadmium, mercury and lead. Maximum contaminant levels are set by the EPA and represent the point at which toxic metals render the water no longer safe for humans to drink.²

The Animas and San Juan Rivers provide drinking and irrigation water for many communities. Fortunately backup water sources unconnected to the river were used once the spill was reported. As time goes on, the constant flows of the Animas and San Juan rivers will eventually dilute toxic metal concentrations to much lower levels. Unfortunately, even at much lower levels these toxins will still pose a threat to humans and wildlife, as they tend to accumulate in the river sediment and are released during high water events. Currently, the EPA is assessing at what point the rivers can be opened back up for both drinking and recreation.

Arsenic, lead, mercury and cadmium are considered to be the 1^st, 2^nd, 3^rd, and 7^th most hazardous substances according to the Agency for Toxic Substances and Disease Registry’s (ATSDR) Priority List of Hazardous Substances.³ It is not possible to know if you are being exposed to these toxic metals because they are colorless and odorless in water, plants, and animals that are on the human food chain. Detecting arsenic, cadmium, mercury, and lead in water is not possible without complex analytical equipment. These toxic metals will accumulate in crops irrigated with contaminated water and in fish residing in the river, and enter into aquifers that supply water for both irrigation and drinking.

While river and well water can be tested to determine if it is safe to drink, the only way to know what humans are actually being exposed to is by testing biological specimens such as urine and blood. Lead and organic mercury are commonly tested using whole blood, while arsenic, cadmium, and inorganic mercury are commonly tested using urine.

ZRT has developed a dried urine test that is ideal for assessing individual exposure to arsenic and mercury that may have been consumed in water and in foods grown in contaminated water such as the recent Colorado Mine spill. (Coming in September, ZRT will be adding cadmium to this profile.) We are also currently working on tests (available 2016) that measure lead, cadmium, and mercury in dried blood spot derived from a simple finger prick.

Overexposure to these toxic heavy metals is associated with myriad health issues including cardiovascular disease, cancer, diabetes, and premature aging. Knowing your body burden of these toxic heavy metals through urine testing or blood testing is key to avoiding them in contaminated water and food and preventing health issues associated with overexposure.

Related Resources

References

[1] United States Environmental Protection Agency. Emergency Response to August 2015 Release from Gold King Mine. Available at: http://www2.epa.gov/goldkingmine

[2] United States Environmental Protection Agency. Drinking Water Contaminants. Available at: http://water.epa.gov/drink/contaminants/index.cfm#List

[3] Agency for Toxic Substances & Disease Registry. Priority List of Hazardous Substances. Available at: http://www.atsdr.cdc.gov/SPL/index.html

Arsenic Exposure from Rice and Rice-Based Breakfast Cereals

Wed, 19 Nov 2014 23:19:00 -0800

Did you know that the amount of arsenic in your public water supply is strictly regulated by the FDA, and must test below 10 ppb* total arsenic? Ironically, the food we eat has no such regulations on arsenic content, and some staple foods such as rice may contain high levels of arsenic.

Arsenic is a natural element found in soil and water at different concentrations throughout the world. There are two types of arsenic, inorganic and organic, the former being much more toxic and associated with generation of free radicals that damage tissues and potentially lead to diseases of aging and cancer. Typically, chronic long term arsenic exposure comes from private or unregulated wells, but recently rice grown in soil and irrigation water containing high levels of arsenic has been identified as a major source of arsenic exposure.

How much arsenic did Consumer Reports find in popular rice-based food products? Total levels of arsenic reached as high as 963 ppb, while inorganic arsenic levels topped out at 222 ppb. Most products had inorganic arsenic levels between 50 and 150 ppb. Americans eat on average 25 pounds of rice a year (compared to 210 in China and 365 in Vietnam). Assuming consumption of 25 pounds of rice products a year with an inorganic arsenic concentration of 100 ppb, exposure would equate to over 1000 µg per year. This might not be of concern in the short term, but persistent exposure to inorganic arsenic over a long period of time is detrimental to health.

What makes arsenic so toxic? Exposure to arsenic results in the formation of reactive oxygen species (ROS) which cause oxidative damage, primarily to DNA and mitochondria. Arsenic also forms a tight complex with selenium, reducing its bioavailability for incorporation into selenoproteins. Selenoproteins play important roles in thyroid hormone synthesis and as antioxidants to protect tissues against attack by reactive oxygen species (ROS), leading to carcinogenesis. Chronic arsenic exposure, especially in the presence of selenium deficiency, can therefore contribute to both hypothyroidism and an increased risk of cancer.

Unfortunately there is no way of knowing if you are consuming too much arsenic or too little selenium in your food, unless you test a body fluid that reflects exposure to these toxic and essential elements. Arsenic has no taste, smell, or color, which makes it nearly impossible to know if the water you are drinking, or the food you are eating contains too much arsenic.

To overcome this hurdle, ZRT Laboratory has developed a simple urine test to evaluate consumption of arsenic. Urine is collected on a filter strip and dried prior to shipping to ZRT, making collection and shipping simple and convenient.

So, before you pick up that bag of rice, rice crispy treat, or box of riced-based cereal, stop to think how much arsenic you might be exposing yourself and your family members to, and if selenium is high enough to counter the toxic effects of arsenic as well as other heavy metals like mercury.

*Parts per billion [ppb] = µg of analyte per liter of solution = µg of analyte per kilogram of solid

Related Resources

References:

Consumer Reports. Results of our tests of rice and rice products. Consumer Reports, November 2012. Available at: http://consumerreports.org/content/dam/cro/magazine-articles/2012/November/Consumer Reports Arsenic in Food November 2012_1.pdf

Report: Arsenic Found in Common Breakfast Cereals. REALfarmacy.com 2014, Nov 7th. Available at: http://www.realfarmacy.com/report-arsenic-found-in-common-breakfast-cereals/#!prettyPhoto.

Jomova K, Jenisova Z, Feszterova M, Baros S, Liska J, Hudecova D, Rhodes CJ, Valko M. Arsenic: toxicity, oxidative stress and human disease. J Appl Toxicol. 2011;31(2):95-107.