Vitamin B12 for Vegans and Absorption Issues

Table of Contents

1. Vegan Deficiency Is Common Without Supplements
2. Nori, Spirulina, and the Inactive-Analogue Problem
3. Proton Pump Inhibitors and H2 Blockers
4. Metformin-Induced B12 Deficiency
5. Atrophic Gastritis in the Elderly
6. Post-Bariatric and Gastric Surgery
7. Supplementation Strategies by Risk Group
8. The Methylcobalamin vs Cyanocobalamin Debate
9. Cautions
10. Key Research Papers
11. Connections
12. Featured Videos

Vegan Deficiency Is Common Without Supplements

B12 is the only vitamin that cannot be reliably obtained from any plant food. The reason is biological: B12 is produced exclusively by certain bacteria and archaea, not by plants or animals. Animals that eat B12-producing bacteria (or eat other animals that did) accumulate B12 in their tissues. Plants do not.

The clinical consequence: any diet that excludes all animal foods (meat, fish, eggs, dairy) without supplementation will eventually produce B12 deficiency. The timeline depends on starting reserves (healthy adults store 2-5 mg of B12 in the liver, which is enough for 3-5 years of demand), but the trajectory is the same: serum B12 falls, then methylmalonic acid (MMA) rises, then symptoms appear.

The evidence is consistent across studies:

• A 2014 review of 40 studies that measured serum B12 in vegetarians found deficiency in 0–86.5% of adults and elderly people, with higher rates in vegans than in other vegetarians; deficiency reached 45% in infants, 0–33.3% in children and adolescents, and 17–39% in pregnant women, depending on the trimester (Pawlak and colleagues, 2014). Vegans who took no B12 supplements were at especially high risk.
• Even self-described "well-supplemented" vegans frequently have inadequate B12 status when measured rigorously with methylmalonic acid and holoTC
• Infants born to and breastfed by B12-deficient vegan mothers can develop severe, sometimes irreversible neurological injury within months of birth — this is a recognized medical emergency described in pediatric case reports from around the world
• Long-term vegetarians (lacto-ovo) have lower but still meaningfully elevated rates of B12 deficiency compared to omnivores — egg and dairy consumption alone is usually insufficient unless intake is high and regular

The bottom line, accepted by every major nutrition society including the Academy of Nutrition and Dietetics (US), the British Dietetic Association, the German Society for Nutrition, and the Vegan Society itself: every strict vegan must supplement B12, without exception.

Supplement practice commonly described for vegans:

• Methylcobalamin or cyanocobalamin 250-1000 mcg daily, or 2000 mcg twice weekly
• Sublingual or oral routes are equivalent for most people
• Check serum B12 + methylmalonic acid every 1-2 years to confirm adequacy
• In pregnancy and breastfeeding, B12 needs are higher (the Institute of Medicine RDA is 2.6 µg a day in pregnancy and 2.8 µg in breastfeeding, against 2.4 µg for other adults), and the infant depends entirely on the mother's B12 status
• The Institute of Medicine adequate intake for infants is 0.4 µg a day from birth to 6 months and 0.5 µg a day from 7 to 12 months, and it states that infants of vegan mothers should be supplemented with B12 at the adequate intake from birth, because their stores at birth are low and their mother's milk may supply very small amounts

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Nori, Spirulina, and the Inactive-Analogue Problem

The persistent claim that certain plant foods — particularly nori, spirulina, chlorella, tempeh, miso, and other fermented foods — contain "natural" B12 sufficient for vegan needs is common in alternative nutrition. The truth is more complicated.

Most B12 measurements use microbiological assays or chemiluminescence assays that detect "corrinoids" — molecules with the cobalt-corrin ring structure of B12. The problem is that not all corrinoids are bioactive in humans. Bacteria produce many different corrinoid variants, some of which have minor chemical modifications that prevent them from binding to human intrinsic factor and methionine synthase. These molecules show up as "B12" on standard assays but cannot fulfill B12's metabolic role — they are called inactive B12 analogues or pseudovitamin B12.

Specifics:

• Spirulina — up to 80% of its measured "B12" is pseudovitamin B12. The remaining 20% that is bioactive is in small enough amounts that spirulina cannot reliably meet B12 needs. Worse, the inactive analogues may actually compete with true B12 for binding sites, potentially worsening deficiency. Spirulina is not a reliable B12 source.
• Chlorella — some chlorella strains do contain detectable bioactive B12 (apparently of bacterial origin from the culture medium), but the amounts vary widely between batches and producers, and clinical reliability is poor.
• Nori (Porphyra) — dried nori (purple laver) contains bioactive B12. A 2014 review found that about 4 g of dried purple laver (77.6 µg of B12 per 100 g dry weight) supplies the adult RDA of 2.4 µg a day, that nori B12 was bioavailable in rats, and that seasoned and toasted laver products contain less; it described nori as the most suitable B12 source presently available for vegetarians (Watanabe and colleagues, 2014).
• Fermented foods (tempeh, miso, sauerkraut, kimchi) — tempeh, a fermented soybean food, can contain a considerable amount of B12, 0.7–8.0 µg per 100 g, probably from bacteria during its production; other fermented soybean products contain minute amounts, and kimchi only traces, under 0.1 µg per 100 g (Watanabe and colleagues, 2014).
• Mushrooms — some mushroom varieties (especially shiitake grown on B12-enriched substrates) contain small amounts of B12, but again the amounts are insufficient and inconsistent.
• Fortified plant milks, fortified nutritional yeast, fortified breakfast cereals — these contain added cyanocobalamin or methylcobalamin and are reliable sources. Read the label: unfortified nutritional yeast contains no B12.

The take-home message: fortified foods and supplements are the most dependable B12 sources for vegans; among whole plant foods, nori and tempeh contain the most B12, in amounts that vary between products.

This is not a controversial statement among practicing nutrition scientists. It is one of the rare topics in nutrition where the evidence is so clear and so consistent that even the most plant-positive organizations agree.

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Proton Pump Inhibitors and H2 Blockers

Proton pump inhibitors (PPIs) — omeprazole, esomeprazole, lansoprazole, pantoprazole, rabeprazole, dexlansoprazole — and H2 receptor blockers — famotidine, ranitidine (now withdrawn in many countries), nizatidine, cimetidine — reduce gastric acid output. They are among the most commonly prescribed medications in the world, used for gastroesophageal reflux disease (GERD), peptic ulcer disease, Barrett's esophagus, prevention of nonsteroidal anti-inflammatory drug (NSAID)-related ulcers, and many other indications.

Gastric acid is the first essential step in B12 absorption. B12 in food is bound to proteins; gastric acid plus pepsin liberates B12 from these protein carriers so it can bind to haptocorrin and proceed through the absorption cascade. When gastric acid is suppressed, this liberation step fails. Synthetic B12 in supplements (already free, not protein-bound) bypasses this problem — only food-bound B12 absorption is impaired.

Clinical implications:

• Two or more years of proton pump inhibitor use was associated with B12 deficiency (odds ratio 1.65) in a large case-control study in Kaiser Permanente Northern California that compared 25,956 people with B12 deficiency and 184,199 without (Lam and colleagues, 2013)
• The effect is dose-dependent and duration-dependent — in the same study, more than 1.5 PPI pills a day carried a stronger association (odds ratio 1.95) than under 0.75 pills a day (odds ratio 1.63)
• H2 blockers carry a similar but typically smaller risk because their acid suppression is less complete (odds ratio 1.25 for 2 or more years in the same study)
• Older adults on proton pump inhibitors are at particularly elevated risk because their baseline B12 absorption is already reduced by age-related atrophic gastritis

Management described in clinical and nutrition practice:

• A yearly B12 check for people on proton pump inhibitors for more than a year
• Daily supplemental B12 (250-1000 mcg) is appropriate prophylaxis for long-term proton pump inhibitor users — this bypasses the absorption problem because synthetic B12 doesn't need to be liberated from food
• Consider periodic proton pump inhibitor deprescribing trials — many patients can step down to H2 blockers or to as-needed proton pump inhibitor use, reducing the chronic absorption impairment
• Methylcobalamin, hydroxocobalamin, or cyanocobalamin all work for proton pump inhibitor users — the form is less important than the consistent daily supplementation

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Metformin-Induced B12 Deficiency

Metformin is the most widely prescribed diabetes medication worldwide and the first-line drug for type 2 diabetes. It also reduces B12 absorption through a complex mechanism that appears to involve calcium-dependent disruption of the cubilin-amnionless receptor in the terminal ileum. Long-term metformin users develop B12 deficiency at rates of approximately 10-30% depending on duration, dose, and the diagnostic threshold used.

The clinical risk is particularly important because:

• Metformin is taken long-term — often for decades
• The diabetic patient population is already at high risk for peripheral neuropathy (from the diabetes), and B12 deficiency adds an entirely separate cause of peripheral neuropathy
• The neuropathy that develops is frequently attributed to "diabetic neuropathy" when in reality some or all of it is B12 deficiency from the metformin
• B12 deficiency is treatable; diabetic neuropathy is much harder to treat

The American Diabetes Association now recommends periodic B12 monitoring for all patients on long-term metformin, particularly those with peripheral neuropathy, anemia, or other suggestive findings.

Management described in clinical and nutrition practice:

• The metformin label reports that in 29-week trials about 7% of patients developed low B12 levels, and it states that blood counts should be measured every year and vitamin B12 at 2- to 3-year intervals in people taking metformin
• Consider routine B12 supplementation (500-1000 mcg/day) for any patient on metformin >1 year, particularly older adults and those with elevated methylmalonic acid
• If neuropathic symptoms develop in a metformin-treated diabetic patient, check B12 and methylmalonic acid before assuming the symptoms are from the diabetes — the B12-deficient subgroup may have completely reversible symptoms with repletion
• Calcium supplementation (1200-1500 mg/day) has been shown to partially reverse the metformin-induced B12 malabsorption — the mechanism is thought to involve calcium-dependent restoration of the ileal receptor function. It is used alongside B12 supplementation, not in place of it

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Atrophic Gastritis in the Elderly

Atrophic gastritis — the thinning and partial loss of the gastric glandular lining — affects an estimated 10 to 30% of people older than 50 (Institute of Medicine, 1998). The condition is often asymptomatic but produces clinically meaningful reduction in gastric acid secretion and intrinsic factor production. It is the most common cause of B12 deficiency in the elderly and a major contributor to the broader picture of late-life cognitive decline, peripheral neuropathy, and fatigue.

Causes of atrophic gastritis:

• Autoimmune (pernicious anemia) — the body-predominant type with anti-parietal-cell and anti-intrinsic-factor antibodies
• H. pylori-related — the antrum-predominant type from chronic H. pylori infection that has eradicated the gastric glandular tissue over years; an underappreciated cause of B12 deficiency in older adults with prior H. pylori exposure
• Environmental / age-related — the multifactorial type that develops gradually with aging without a clear single cause

Clinical presentation: often nothing — many patients are entirely asymptomatic. When symptoms occur, they may include dyspepsia, early satiety, postprandial fullness, and slow gastric emptying. The clinical hallmark of severe atrophic gastritis is its consequences: B12 deficiency, iron deficiency (from impaired acid-dependent iron solubilization), reduced absorption of other micronutrients, and elevated gastric cancer risk.

Diagnosis: serum gastrin (markedly elevated in autoimmune atrophic gastritis), pepsinogen I (low) and pepsinogen I/II ratio (suppressed), anti-IF and anti-parietal-cell antibodies, and confirmatory upper endoscopy with body and antrum biopsies. A combined blood test of gastrin-17, pepsinogen I, pepsinogen II, and anti-H. pylori antibodies can stratify atrophic gastritis risk without requiring endoscopy.

Management for B12: the same as for pernicious anemia — lifelong B12 supplementation, either parenteral or high-dose oral. The atrophic gastritis itself is generally not reversible (though H. pylori eradication can stop progression and sometimes produce partial regeneration), but the B12 deficiency it causes is fully treatable.

Testing: B12 (with methylmalonic acid if borderline) is a low-cost blood test for anyone over 60 with unexplained fatigue, peripheral neuropathy, cognitive decline, or unexplained anemia. The cost is trivial and the diagnostic yield is meaningful.

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Post-Bariatric and Gastric Surgery

Bariatric surgery (Roux-en-Y gastric bypass, sleeve gastrectomy, biliopancreatic diversion) fundamentally alters B12 absorption anatomy. The mechanisms vary by procedure:

• Roux-en-Y gastric bypass — bypasses most of the stomach (reduced acid and intrinsic factor production) and the duodenum/proximal jejunum, with the food stream rejoining the digestive enzymes in the mid-jejunum. The combined acid + IF + transit-time effect is substantial. B12 deficiency develops in 30-50% of patients within 5 years if not supplemented.
• Sleeve gastrectomy — removes a large portion of the stomach (reducing acid and IF) but preserves the rest of the gastrointestinal (GI) tract. B12 deficiency is less common than after Roux-en-Y but still elevated, with rates of 10-20% over 5 years.
• Biliopancreatic diversion (now uncommon) — severe macro- and micronutrient malabsorption; high rates of multiple vitamin and mineral deficiencies including B12.
• Subtotal or total gastrectomy (for gastric cancer or severe ulcer disease) — eliminates intrinsic factor production entirely. Lifelong B12 supplementation is mandatory, equivalent to pernicious anemia management.

Universal recommendation: all post-bariatric patients require lifelong B12 supplementation. Standard protocols:

• Sublingual or oral methylcobalamin/cyanocobalamin 1000-2000 mcg daily, OR
• Intramuscular hydroxocobalamin 1000 mcg every 1-3 months
• Annual B12 monitoring + methylmalonic acid + complete blood count (CBC)
• Concurrent iron, calcium + vitamin D, and other micronutrient monitoring (these patients are at risk for multiple deficiencies, not just B12)

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Supplementation Strategies by Risk Group

The amounts and testing intervals below are common supplement practice; official figures are given where they exist.

Healthy Omnivore (Maintenance / Insurance)

• Optional B-complex supplement containing 100-500 mcg B12 several times weekly
• Most healthy omnivores who eat meat, fish, dairy, and eggs regularly get enough B12 from food
• Consider checking serum B12 once in middle age to establish a baseline

Vegetarian (Lacto-Ovo)

• Methylcobalamin or cyanocobalamin 250-500 mcg daily, or 1000 mcg several times weekly
• Check serum B12 + methylmalonic acid every 2-3 years
• Particularly important if egg/dairy consumption is sporadic

Vegan

• Methylcobalamin or cyanocobalamin 250-1000 mcg daily, OR 2000 mcg twice weekly
• Check serum B12 + methylmalonic acid every 1-2 years (every 6-12 months in pregnancy / lactation)
• Mandatory for life — no exceptions

Long-term Proton Pump Inhibitor / H2 Blocker User

• Methylcobalamin or cyanocobalamin 500-1000 mcg daily (bypasses acid-dependent absorption step)
• Annual B12 + methylmalonic acid monitoring
• Periodic deprescribing trial to reduce or eliminate proton pump inhibitor use if clinically feasible

Long-term Metformin User

• Methylcobalamin or cyanocobalamin 500-1000 mcg daily
• Periodic B12 testing: the American Diabetes Association (ADA) Standards of Care note that metformin is associated with increased risk of B12 deficiency and suggest periodic testing of B12 levels; the metformin label gives 2- to 3-year intervals
• Consider calcium 1200 mg/day for partial restoration of ileal absorption

Adults Over 60

• Methylcobalamin or cyanocobalamin 250-500 mcg daily is a common supplement amount. The Institute of Medicine sets the RDA at 2.4 µg a day and, because 10 to 30% of older people may be unable to absorb the B12 naturally present in food, advises people older than 50 to meet it mainly from B12-fortified foods or a B12-containing supplement
• Periodic B12 + methylmalonic acid monitoring, every 2-3 years
• If cognitive symptoms, fatigue, or neuropathy emerges, check B12 status promptly

Pernicious Anemia

• Initial IM hydroxocobalamin/methylcobalamin daily for 1-2 weeks, then weekly for 4-8 weeks
• Maintenance: IM hydroxocobalamin 1000 mcg every 1-3 months, OR daily high-dose oral methylcobalamin 2000 mcg
• Lifelong; never stop
• Periodic monitoring of B12, methylmalonic acid, complete blood count, thyroid function
• Endoscopic gastric cancer surveillance every 3-5 years

Post-Bariatric Surgery

• Sublingual or oral methylcobalamin 1000-2000 mcg daily, OR IM hydroxocobalamin every 1-3 months
• Annual B12 + methylmalonic acid + complete blood count + iron studies + vitamin D + parathyroid hormone
• Lifelong

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The Methylcobalamin vs Cyanocobalamin Debate

One of the most persistent debates in the natural medicine community concerns the choice between methylcobalamin (the methylated coenzyme form) and cyanocobalamin (the synthetic, cyanide-containing form) for general supplementation. Both reach essentially the same end — raising tissue B12 levels — but they take different paths to get there.

The case for methylcobalamin:

• Already in the active coenzyme form — no metabolic conversion required
• Directly participates in the methionine synthase reaction
• Preferred in patients with neurological involvement (per the integrative neurology literature)
• Preferred in smokers (no cyanide load)
• Preferred in patients with renal impairment (slowed cyanide clearance)
• Preferred in patients with methylenetetrahydrofolate reductase (MTHFR) variants or chronic methylation issues
• Has slightly better tissue retention in some pharmacokinetic studies

The case for cyanocobalamin:

• Vastly more studied — nearly all of the 60+ years of clinical evidence for B12 therapy used cyanocobalamin
• Substantially cheaper (often 5-10x less expensive than methylcobalamin)
• More stable in storage (less degradation from light, heat, oxygen)
• Equally effective at raising serum B12 and correcting hematological deficiency
• The "cyanide" concern is overstated — the amount of cyanide released from a 1000 mcg dose is approximately 20 mcg, which is trivial compared to the daily cyanide exposure from food (almonds, apricot kernels, leafy greens contain measurable cyanide naturally)

The case for hydroxocobalamin:

• Naturally occurring form (produced by bacteria, including those in the gut)
• Longest tissue retention — the standard for IM injection in Europe
• No cyanide concern
• Scavenges excess nitric oxide (relevant for some inflammatory conditions)
• Now available in many countries as the IM injection of choice

Practical resolution:

• For healthy people with no special concerns: any form works. Choose based on cost and availability.
• For neurological involvement, methylenetetrahydrofolate reductase variants, smokers, renal impairment, or "biochemical sensitivity": methylcobalamin or hydroxocobalamin preferred over cyanocobalamin.
• For IM injection: hydroxocobalamin preferred (longer interval between doses) but cyanocobalamin also acceptable.
• For maximum natural medicine pedigree: hydroxocobalamin (the bacterial-natural form).
• The choice matters less than consistent supplementation — taking any form of B12 reliably every day is far better than choosing the "perfect" form and missing doses.

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Cautions

• Vegan pregnancy and infants — the highest-stakes B12 scenario. Vegan and unsupplemented vegetarian mothers can have infants with severe, sometimes permanent neurological injury within months of birth. The infant depends on the mother's B12 through pregnancy and breastfeeding. The Institute of Medicine states that infants of vegan mothers should be supplemented with B12 at the adequate intake from birth: 0.4 µg a day from birth to 6 months and 0.5 µg a day from 7 to 12 months.
• Spirulina, chlorella, and unfortified nutritional yeast are not dependable B12 sources — spirulina's B12 is mostly the inactive pseudovitamin form and unfortified nutritional yeast contains none; nori and tempeh contain real B12, in amounts that vary between products (see above).
• B12 can be corrected while the drug continues — proton pump inhibitors and metformin treat serious conditions. The metformin label states that the fall in B12 appears to be rapidly reversible with B12 supplementation, and supplemental B12 bypasses the acid-dependent step that proton pump inhibitors block (see above).
• Combined deficiencies — vegans, atrophic gastritis patients, post-bariatric patients, and the elderly are at risk for multiple deficiencies (iron, vitamin D, calcium, zinc, omega-3, vitamin B6, vitamin B2) not just B12. A comprehensive nutritional assessment is warranted.
• Methylated forms can occasionally cause overstimulation — in patients with COMT slow variants or histamine sensitivity, high-dose methylcobalamin (especially combined with high-dose methylfolate) can produce anxiety, insomnia, or irritability. Practitioners start at the lower end and increase gradually.
• Acne flares — rarely, high-dose B12 (cyanocobalamin in particular) can trigger acne or rosacea flares. Switching to methylcobalamin or hydroxocobalamin usually resolves the issue.
• Nitrous oxide — B12 deficiency is precipitated or worsened by nitrous oxide exposure (recreational "whippets" or repeated dental anesthesia). People whose B12 status is already marginal are the most vulnerable, both with planned N2O exposure and with recreational use.

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Key Research Papers

1. Pawlak R, Lester SE, Babatunde T (2014). The prevalence of cobalamin deficiency among vegetarians assessed by serum vitamin B12: a review of literature. Eur J Clin Nutr. 68(5):541-8. — PubMed PMID: 24667752
2. Watanabe F (2007). Vitamin B12 sources and bioavailability. Exp Biol Med. — the canonical review of plant B12 analogue issues. — PubMed
3. Watanabe F, Katsura H, Takenaka S, et al. (1999). Pseudovitamin B(12) is the predominant cobamide of an algal health food, spirulina tablets. J Agric Food Chem. 47(11):4736-41. — PubMed PMID: 10552882
4. Lam JR et al. (2013). Proton pump inhibitor and histamine 2 receptor antagonist use and vitamin B12 deficiency. JAMA. — a case-control study (25,956 cases, 184,199 controls) finding an association between 2 or more years of acid-suppressing drugs and B12 deficiency. — PubMed PMID: 24327038
5. de Jager J et al. (2010). Long term treatment with metformin in patients with type 2 diabetes and risk of vitamin B-12 deficiency: randomised placebo controlled trial. BMJ. — PubMed PMID: 20488910
6. Aroda VR et al. (2016). Long-term metformin use and vitamin B12 deficiency in the Diabetes Prevention Program Outcomes Study. J Clin Endocrinol Metab. — PubMed
7. Allen LH (2009). How common is vitamin B-12 deficiency? Am J Clin Nutr. — PubMed
8. Andres E et al. (2004). Vitamin B12 (cobalamin) deficiency in elderly patients. CMAJ. — PubMed PMID: 15289425
9. Russell RM (1992). Changes in gastrointestinal function attributed to aging. Am J Clin Nutr. — atrophic gastritis epidemiology in the elderly. — PubMed PMID: 1590257
10. Stein J et al. (2014). The nutritional and pharmacological consequences of obesity surgery. Aliment Pharmacol Ther. — PubMed
11. Rizzo G et al. (2016). Vitamin B12 among vegetarians: status, assessment and supplementation. Nutrients. — PubMed PMID: 27916823
12. Watanabe F, Yabuta Y, Bito T, Teng F (2014). Vitamin B12-containing plant food sources for vegetarians. Nutrients. 6(5):1861-73. — PubMed PMID: 24803097
13. American Diabetes Association Professional Practice Committee for Diabetes (2026). 9. Pharmacologic approaches to glycemic treatment: Standards of Care in Diabetes—2026. Diabetes Care. 49(Suppl 1):S183-S215. — PubMed PMID: 41358900
14. Institute of Medicine (1998). Dietary Reference Intakes for Thiamin, Riboflavin, Niacin, Vitamin B6, Folate, Vitamin B12, Pantothenic Acid, Biotin, and Choline, chapter 9: Vitamin B12. Washington, DC: National Academies Press. — doi:10.17226/6015
15. Metformin hydrochloride tablets, US prescribing information, section 5.2 Vitamin B12 Deficiency. DailyMed, US National Library of Medicine. — DailyMed: metformin hydrochloride tablets label
16. Wile DJ, Toth C (2010). Association of metformin, elevated homocysteine, and methylmalonic acid levels and clinically worsened diabetic peripheral neuropathy. Diabetes Care. — PubMed PMID: 19846797

PubMed Topic Searches

1. PubMed: vegan vegetarian B12 deficiency
2. PubMed: spirulina pseudovitamin B12
3. PubMed: PPI B12 deficiency
4. PubMed: metformin B12 deficiency long-term
5. PubMed: atrophic gastritis elderly B12 iron
6. PubMed: methylcobalamin vs cyanocobalamin

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Connections

• All Vitamins
• Vitamin B12’s Impossible Journey — interactive animation
• Vitamin B12 Overview
• B12 Benefits Hub
• B12 for Nerve Health
• B12 for Anemia
• B12 for Cognition & Methylation
• B12 Deficiency Diagnosis
• B12 and Nervous System
• Vitamin B12 Test
• Homocysteine
• Complete Blood Count
• Anemia
• Small Intestinal Bacterial Overgrowth
• Celiac Disease
• Crohn's Disease
• Diabetes (Metformin)
• Metformin — blocks B12 uptake at the ileal receptor.
• Organ Meats
• Eggs
• Salmon
• Nutritional Yeast
• Deficiency
• Toxicity
• History
• Sources

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