What is molybdenum

Molybdenum is a heavy metallic element found naturally throughout the environment and is also used by industries to manufacture a wide range of common products. Molybdenum is widely distributed in nature, the abundance in the earth’s crust being about 1-1.5 mg molybdenum/kg 1). Molybdenum is ubiquitous in food and water as soluble molybdates (Mo(VI)O42-). Molybdenum is required as a component of enzymes involved in the catabolism of sulphur amino acids and heterocyclic compounds, as well as in the metabolism of aromatic aldehydes. Because of its role in metabolism, molybdenum is considered an essential dietary element for mammals, though clinical signs of dietary molybdenum deficiency in otherwise healthy humans have not been described 2). Molybdenum is a refractory metallic element used principally as an alloying agent in steel, cast iron, and superalloys to enhance hardenability, strength, toughness, and wear and corrosion resistance 3). To achieve desired metallurgical properties, molybdenum, primarily in the form of molybdic oxide or ferromolybdenum, is frequently used in combination with or added to chromium, manganese, niobium, nickel, tungsten, or other alloy metals. The versatility of molybdenum in enhancing a variety of alloy properties has ensured it a significant role in contemporary industrial technology, which increasingly requires materials that are serviceable under high stress, expanded temperature ranges, and highly corrosive environments. Moreover, molybdenum finds significant usage as a refractory metal in numerous chemical applications, including catalysts, lubricants, and pigments 4). There is little substitution for molybdenum in its major application in steels and cast irons. In fact, because of the availability and versatility of molybdenum, industry has sought to develop new materials that benefit from its alloying properties.

In humans, molybdenum is also an essential trace element, being a component of the enzymes xanthine oxidoreductase, sulphite oxidase, aldehyde oxidase, nitrate reductase and mitochondrial amidoxime reducing component require molybdenum linked with a pterin (molybdopterin) as the cofactor 5). These enzymes are involved in the metabolism of aromatic aldehydes and the catabolism of sulphur-containing amino acids and heterocyclic compounds, including purines, pyrimidines, pteridins and pyridines.

Molybdenum-containing enzymes catalyse redox reactions and are found in many plants and animal organisms. As a consequence of the easy interconvertibility of different oxidation states (Mo4+/Mo6+), molybdenum-containing enzymes have the ability to provide electron transfer pathways. In addition to molybdenum, they also contain other prosthetic groups such as flavin adenine dinucleotide or haeme 6).

Molybdenum cofactor is synthesized in the cytosol by a conserved biosynthetic pathway that can be divided into four main steps. In the final step of molybdenum cofactor biosynthesis, a single molybdenum ion is bound to one or two molybdopterin dithiolates. After completion of biosynthesis, mature molybdenum cofactor has to be inserted into molybdoenzymes. A molybdenum cofactor carrier protein has been described in the green alga Chlamydomonas rheinhardtii, but information is lacking for other eukaryotes 7). The formation of active molybdoenzymes depends not only on the availability of molybdenum but also on the presence of iron, zinc and copper 8).

The US Institute of Medicine 9) derived an average requirement based on a molybdenum balance study with four young males by Turnlund et al. 10). Average molybdenum balance was achieved with an intake of 22 μg/day, and no clinical signs of deficiency or biochemical changes associated with molybdenum deficiency were observed. The average minimum molybdenum requirement for maintaining adequate molybdenum status was estimated to be 22 μg/day, to which an additional 3 μg/day was added to allow for miscellaneous losses. In addition, it was assumed that molybdenum bioavailability from some diets may be lower than from the diet provided in the study. Thus, an average bioavailability of 75 % was used to set an Estimated Average Requirement (EAR) of 34 μg/day. Because of the use of only two different molybdenum intake levels and the small size of the study, US Institute of Medicine 11) used a coefficient of variation of 15 % and derived a Recommended Dietary Allowance (RDA) of 45 μg/day as the Estimated Average Requirement (EAR) plus twice the coefficient of variation to cover the needs of 97 to 98 % of the individuals in the group. As no data on which to base an Estimated Average Requirement (EAR) were found for women or older adults, the same values were given for these population groups 12).

Table 1. Recommended Dietary Allowances (RDAs) for molybdenum

Birth to 6 months2 mcg*2 mcg*
7–12 months3 mcg*3 mcg*
1–3 years17 mcg17 mcg
4–8 years22 mcg22 mcg
9–13 years34 mcg34 mcg
14–18 years43 mcg43 mcg50 mcg50 mcg
19+ years45 mcg45 mcg50 mcg50 mcg

Footnote: * Adequate Intake (AI): Intake at this level is assumed to ensure nutritional adequacy; established when evidence is insufficient to develop an RDA. Adequate Intake (AI) based on mean molybdenum intakes of infants fed primarily human milk.

[Source 13) ]

Figure 1. Molybdenum cofactor

molybdenum cofactor
[Source 14) ]

Molybdenum supplements

Molybdenum is also available in dietary supplements containing molybdenum only, in combination with other minerals, and in multivitamin/multimineral products. Amounts range from about 50 mcg to 500 mcg. Forms of molybdenum in dietary supplements include molybdenum chloride, sodium molybdate, molybdenum glycinate, and molybdenum amino acid chelate 15). No studies have compared the relative bioavailability of molybdenum from these different forms.

Molybdenum foods

Molybdenum is present in nearly all foods in trace amounts as soluble molybdates.

Foods high in molybdenum are:

  • Pulses, cereal grains and grain products, offal (liver, kidney) and nuts
  • Organ meats, whole grains, green leafy vegetables, milk, beans

Molybdenum is widespread in the diet. In plant foods, molybdenum content is primarily determined by the regional richness of the soil and in the water used for irrigation and the content in meat depends on forage of the animals 16) and molybdenum uptake by plants is promoted by neutral or alkaline soils 17). Legumes are the richest sources of molybdenum, with lima beans providing 87 mg molybdenum per 100 g 18). Other foods high in molybdenum include wholegrains, nuts, and beef liver 19). The top sources of molybdenum in U.S. diets are legumes, cereal grains, leafy vegetables, beef liver, and milk 20). Milk and cheese products are the main sources of molybdenum for teens and children 21).

Drinking water generally contains only small amounts of molybdenum 22). However, according to 2017 data from the U.S. Environmental Protection Agency, 0.8% of drinking water samples had molybdenum levels above 40 mcg/L 23), although concentrations as high as 200 μg/L have been reported in areas near mining sites 24). The U.S. Department of Agriculture’s (USDA’s) FoodData Central 25) does not list the molybdenum content of foods or provide lists of foods containing molybdenum. Therefore, the amount of information on molybdenum levels in foods is quite limited.

Currently, potassium molybdate (molybdenum VI) may be added to food supplements 26), whereas ammonium molybdate (molybdenum VI) and sodium molybdate (molybdenum VI) may be added to both foods and food supplements 27).

Cereals and cereal-based products including bread are the major food contributors to the dietary molybdenum intake of adults 28). Mean molybdenum intakes, as assessed in duplicate diet or food portion studies, total diet studies and market basket studies, vary over a wide range, i.e. 58 μg/day to 157 μg/day, for adults in various European countries. Mean intakes are at or above 100 μg/day in five of the eight European countries for which data are available. Molybdenum intakes of children are only available from two European countries.

Infant and follow-on formula: In a report on the essential requirements of infant and follow-on formulae, the Scientific Committee on Food did not define a minimum or maximum content of molybdenum for either type of formulae 29). Compared to mature human milk, cow‟s milk has a higher molybdenum concentration [34 μg/kg as reported by Rose et al. 30), mean of 46 μg/kg as reported by Anses 31)]. Hence, the molybdenum content of cow’s milk based-infant formula is higher compared to mature human milk. For 81 powdered cow’s milk-based or soy-based infant formulae from the US and Canada, molybdenum concentrations ranged from 15.4 to 80.3 μg/L (mean ± SE, 37.7 ± 1.7 μg/L) 32).

Water-soluble molybdates are efficiently and rapidly absorbed from the digestive tract at a wide range of intakes, and the body is able to adapt to this wide intake range by regulating excretion via the urine. At doses up to about 1 mg, molybdenum dissolved in water is completely absorbed into the systemic circulation. Molybdenum absorption in the presence of solid foods (cress, green salad, tomatoes, bean soup) is lower compared to administration with water 33). When added to a beverage containing starch, dextrimaltose, oil, sucrose, α-cellulose and minerals, the absorption efficiency of increasing doses of molybdenum ranging from 24 to 1 378 μg was between 90 and 94 % in healthy men 34). Black tea has been shown to considerably reduce molybdenum absorption upon ingestion of relatively high amounts of molybdenum (0.5-1 mg as a single dose of stable isotope) 35). In ten premature infants, absorption of the stable isotope molybdenum from infant formula was 97.5 % (96.3-99.1 %) after receiving 25 μg molybdenum/kg body weight 36).

Studies using kale or soy intrinsically labeled with stable isotopes of molybdenum have shown that molybdenum absorption was 86.1 % and 56.7 %, respectively, from meals with either kale or soy casseroles containing about 100 μg molybdenum. Molybdenum absorption from an extrinsic label also added to the meals was 87.5 %. When the molybdenum content of the meal was increased to about 310 μg in a subsequent study, molybdenum absorption from soy amounted to 58.3 %, and molybdenum absorption from the extrinsic label was 92.8% 37).

Using a compartmental model based on a molybdenum depletion-repletion study in four men, the mean bioavailability of molybdenum from the experimental diet was predicted to be 76 % 38). A slightly higher bioavailability of 83 % for food-bound molybdenum was predicted with the compartmental model, based on a study which gave the same three-day rotating diet regimen but with five different molybdenum contents consecutively for 24 days each to four men 39).

Little is known about the mechanism of molybdenum absorption and the site of absorption in the gastrointestinal tract. In animals, molybdenum (VI) but not molybdenum (IV) is readily absorbed from the duodenum and proximal jejunum 40). Recently, a family of proteins probably related to molybdate transport in animals and humans has been described, though the exact location of this high-affinity transporter within the cell has not yet been identified 41). It is assumed that in addition to a possible high-affinity uptake system, molybdate may also enter the cell nonspecifically through the sulphate uptake system, which has been shown to be present in plants 42).

Tungsten is known to inhibit molybdenum uptake, and this inhibitory effect has been used in animal studies to induce molybdenum deficiency, but it is not considered relevant for humans because of the rare occurrence of tungsten in the environment and consequently in the food chain 43). In sheep and rats, high sulphate intakes have been shown to inhibit molybdenum absorption, suggesting that both sulphate and molybdenum share a common transport mechanism 44). An interaction with copper has been observed leading to copper deficiency in sheep exposed to high molybdenum intake. In ruminants, excessive intakes of molybdenum lead to formation of thiomolybdate in the sulphide-rich environment of the rumen; thiomolybdate (a molecule where sulphur groups surround a molybdenum centre) is a chelator of copper ions, thereby inhibiting copper absorption 45). By contrast, in humans, clinical symptoms of copper deficiency are largely confined to individuals with rare genetic defects in copper metabolism 46). In four adult males on two sorghum diets providing daily 2.4 mg of copper and 166 μg or 540 μg of molybdenum, respectively, fecal copper excretion was comparable and apparent copper absorption unaffected by molybdenum intake 47).

The highest molybdenum concentrations are found in the liver and kidney. In adults, the liver contains 1.3-2.9 mg molybdenum/kg dry matter, the kidney 1.6 mg/kg dry matter, the lung 0.15 mg/kg dry matter, the brain and muscle 0.14 mg/kg dry matter 48), and for hair concentrations of 0.03 mg/kg (Ochi et al., 2011) have been reported. Total body molybdenum of a “standard man” was calculated to be about 2.3 mg after analysis of tissues from 150 accidental deaths 49), and about 2.2 mg with the use of a compartmental model and fractional transfer coefficients observed at a molybdenum intake of 121 μg/day given for 24 days, and which was considered to be in line with the habitual molybdenum intake of participants prior to the study 50).

Storage of molybdenum in mammals is low, and most tissue molybdenum is thought to be associated with molybdoenzymes, as indicated by the reported absence of detectable molybdenum in the liver tissue of molybdenum cofactor-deficient patients 51). In the liver of fetuses (age: 23 weeks of gestation to term), molybdenum concentrations were more than seven-fold lower compared to adults 52), and such differences have subsequently been interpreted as the absence of molybdenum stores and a low fetal molybdenum requirement 53).

In order to fulfill its biological role, molybdenum must enter the cell and be assembled into a molybdenum cofactor. In eukaryotes, the molybdate transport process and the proteins involved are not fully understood 54).

There are no suitable biomarkers of molybdenum status. Biochemical changes observed in subjects with molybdopterin cofactor deficiency, a genetic disorder, or in the one subject reported with possible molybdenum deficiency, have not been observed in healthy individuals on varying levels of molybdenum intake. Low activity of molybdoenzymes in tissues, or changes in substrate/product relationships, are considered as insufficiently specific to be used as biomarkers of status.

In 1993, the Scientific Committee for Food did not publish Dietary Reference Values for molybdenum. More recently, other authorities have set Dietary Reference Values for molybdenum and these are based on the maintenance of molybdenum homeostasis as measured in balance studies, taking into account molybdenum bioavailability from various food sources, or are based on observed molybdenum intakes with a mixed diet.

Various balance studies have been performed to establish molybdenum requirements. However, only one balance study in adults was considered to be of sufficient duration, and was performed with a constant diet and under controlled conditions. In this study carried out in four men, balance was reported to be near zero from day 49 until day 102 of the depletion period when intakes were as low as 22 μg/day 55). Biochemical changes or symptoms suggestive of molybdenum deficiency were not observed and the possibility that humans may be able to achieve molybdenum balance at even lower intakes cannot be excluded 56). Results of two balance studies with some methodological limitations were reported in children, but these studies cannot be used to derive an average molybdenum requirement for children. Data on molybdenum intakes and health outcomes were unavailable for the setting of DRVs for molybdenum.

As the evidence to derive an Average Requirement and thus a Population Reference Intake, was considered insufficient, an Adequate Intake (AI) is proposed. An Adequate Intake (AI) of 65 μg/day is proposed for adult men and women based on mean molybdenum intakes at the lower end of the wide range of observed intakes from mixed diets in Europe 57). Given the scarcity of data on molybdenum intakes in pregnant and lactating women, it is suggested that the adult Adequate Intake (AI) also applies to pregnant and lactating women 58). For infants from seven months and children, it was decided that an Average Requirement could not be established, and an Adequate Intake (AI) is proposed based on extrapolation from the adult AI using isometric scaling and reference body weights of the respective age groups. The respective AIs vary between 10 μg/day in infants aged 7-11 months and 65 μg/day in adolescent boys and girls 59).

Table 2. Molybdenum content of selected foods

FoodMicrograms (mcg) per servingPercent DV*
Black-eyed peas, boiled, ½ cup288640
Beef, liver, pan fried (3 ounces)104231
Lima beans, boiled, ½ cup104231
Yogurt, plain, low-fat, 1 cup2658
Milk, 2% milkfat, 1 cup2249
Potato, baked, flesh and skin, 1 medium1636
Cheerios cereal, ½ cup1533
Shredded wheat cereal, ½ cup1533
Banana, medium1533
White rice, long grain, cooked, ½ cup1329
Bread, whole wheat, 1 slice1227
Peanuts, dry roasted, 1 ounce1124
Chicken, light meat, roasted, 3 ounces920
Egg, large, soft-boiled920
Spinach, boiled, ½ cup818
Beef, ground, regular, pan-fried, 3 ounces818
Pecans, dry roasted, 1 ounce818
Corn, sweet yellow, cooked, ½ cup613
Cheese, cheddar, sharp,1 ounce613
Tuna, light, canned in oil, 3 ounces511
Potato, boiled without skin, ½ cup49
Orange, medium49
Green beans, boiled, ½ cup37
Carrots, raw, ½ cup24
Asparagus, boiled, ½ cup24

Footnote: *DV = Daily Value. The U.S. Food and Drug Administration (FDA) developed DVs to help consumers compare the nutrient contents of foods and dietary supplements within the context of a total diet. The DV for molybdenum is 45 mcg for adults and children age 4 years and older 60). FDA does not require food labels to list molybdenum content unless molybdenum has been added to the food. Foods providing 20% or more of the DV are considered to be high sources of a nutrient, but foods providing lower percentages of the DV also contribute to a healthful diet.

[Source 61) ]

Molybdenum deficiency

Molybdenum is found in many foods and deficiencies are rare. Molybdenum deficiency has been described in animals and molybdenum deficiency in otherwise healthy humans has not been observed and there are no biomarkers of molybdenum status 62). Various metabolic balance studies have been performed to establish molybdenum requirements.

In humans, only a single case report of a syndrome suggestive of dietary molybdenum deficiency in a patient on total parenteral nutrition for several months has been reported 63). A 24-year-old male patient with Crohn’s disease and short bowel syndrome was on total parenteral nutrition (TPN) lacking in molybdenum for 12 months, at which point he developed a syndrome characterized by tachycardia, tachypnea, severe headache, nausea and vomiting, night blindness, and central scotomas, which progressed to edema, lethargy, disorientation and coma 64). These symptoms were associated with high plasma methionine and low serum uric acid concentrations, as well as reduced urinary concentrations of sulphate, thiosulphate, and uric acid. Whilst modification of the total parenteral nutrition solution by lowering the sulphur load was ineffective, treatment with ammonium molybdate (300 μg/day) resulted in considerable improvement of the clinical symptoms and progressive reversal of the biochemical abnormalities within 30 days 65). Clinical signs of molybdenum deficiency in otherwise healthy humans have not been observed 66).

A distinct molybdenum deficiency syndrome has not been observed in animals when subjected to molybdenum restriction, despite considerable reduction in the activity of molybdoenzymes.

Molybdenum cofactor deficiency 67), a rare autosomal recessive syndrome with a defective hepatic synthesis of molybdenum cofactor, results in deficiency of all molybdoenzymes in humans. This genetic defect, for which three subtypes are known according to the gene affected, has been found in a variety of ethnic groups and all over the world 68). Molybdenum cofactor deficiency is characterized by brain dysfunction (encephalopathy) that worsens over time and usually death at an early age 69). Babies with this condition appear normal at birth, but within a week they have feeding difficulties and develop seizures that do not improve with treatment (intractable seizures). Brain abnormalities, including deterioration (atrophy) of brain tissue, lead to severe developmental delay; affected individuals usually do not learn to sit unassisted or to speak. A small percentage of affected individuals have an exaggerated startle reaction (hyperekplexia) to unexpected stimuli such as loud noises. Other features of molybdenum cofactor deficiency can include a small head size (microcephaly) and facial features that are described as “coarse.” The successful treatment of one affected child with molybdenum cofactor deficiency type A using the first detectable intermediate substance in the biosynthesis pathway of molybdenum cofactor has recently been reported 70). In untreated patients, tests reveal that affected individuals have high levels of chemicals called sulfite, S-sulfocysteine, xanthine, and hypoxanthine in the urine and low levels of a chemical called uric acid in the blood. Because of the serious health problems caused by molybdenum cofactor deficiency, affected individuals usually do not survive past early childhood.

Acute molybdenum toxicity data

Acute molybdenum toxicity is rare, but it can occur with industrial mining and metalworking exposure. Exposure to excess molybdenum levels has been associated with adverse health outcomes. The most sensitive effects appear to be respiratory effects following inhalation exposure to molybdenum trioxide and decreases in body weight, kidney damage, decreases in sperm count, and anemia following oral exposure 71). A systematic review of the available human and laboratory animal health effects database resulted in the following hazard identification conclusions:

  • Respiratory effects are a presumed health effect for humans for molybdenum oxides. Decreases in lung function, dyspnea, and cough were reported in a study of workers exposed to fine or ultrafine molybdenum trioxide dust 72). Another study of workers at a molybdenite roasting facility exposed to molybdenum trioxide and other oxides did not have alterations in lung function 73). In studies of rats and mice exposed to molybdenum trioxide for 2 years, hyaline degeneration of the nasal epithelium, squamous metaplasia of the epiglottis, and chronic inflammation (rats only) were observed 74). However, no effects were observed following a 13-week exposure to similar concentrations 75).
  • Renal effects are a presumed health effect for humans. Several studies have reported renal effects in rats exposed to ≥60 mg/kg/day 76). The effects included hyperplasia of the renal proximal tubules, degeneration, increases in total lipid levels in the kidney, and diuresis and creatinuria.
  • The data were inadequate to conclude whether hepatic, uric acid level, reproductive, or developmental effects will occur in humans.
    • Liver Effects. Liver effects, which consisted of decreases in glycogen content, increases in aminotransferase activities, and increases in lipid content, have been observed at higher doses (≥300mg/kg/day) that are often associated with body weight losses 77). No hepatic effects have been observed at lower (≤60 mg/kg/day) doses 78).
    • Reproductive Effects. Cross-sectional epidemiological studies have reported significant associations between blood molybdenum levels and sperm concentration and morphology 79) or testosterone levels 80). No significant alterations in sperm parameters or estrous cycling were observed in a 90-day rat study 81) or in a 2- generation reproductive toxicity study 82). Studies providing limited information on molybdenum doses and/or the copper content of the diet have reported reproductive effects. Decreases in sperm motility and concentration and increases in sperm morphological changes have been observed in rats exposed to approximately 25 mg molybdenum/kg/day as sodium molybdate 83). Degeneration of the seminiferous tubules was also observed at similar molybdenum doses 84). Effects have also been observed in the female reproductive system (oocyte morphological alterations, abnormal rate of ovulation, and irregularities in the estrous cycle) at ≥1.5 mg molybdenum/kg/day in rats 85).
    • Developmental Effects. Mixed results have been observed in animal developmental toxicity studies. Decreases in the number of live fetuses and fetal growth were observed in rats administered 14 mg molybdenum/kg as sodium molybdate 86). Interpretation of the results of this study is limited by the lack of information on the copper content of the diet and the lack of developmental effects reported in two high-quality studies in which rats were exposed to doses as high as 40 mg molybdenum/kg/day as sodium molybdate 87).
    • Uric Acid Levels. A study of workers at a molybdenite roasting facility exposed to molybdenum trioxide and other oxides reported an increase in serum uric acid levels 88). An increased occurrence of gout-like symptoms and increased blood uric acid levels were also observed in residents living in an area of high molybdenum levels in the soil 89); no alterations in urinary uric acid levels were found in a 10-day experimental study in men 90).
  • Cancer Effects. No increases in the risk of lung cancer were reported in workers who self-reported exposure to molybdenum 91). An increase in alveolar/bronchiolar adenomas or carcinomas was observed in mice exposed to molybdenum trioxide for 2 years 92); in rats chronically exposed to airborne molybdenum trioxide, the incidence of alveolar/bronchiolar adenoma/carcinoma was within the range of historical controls 93). The potential carcinogenicity of molybdenum in humans has not been evaluated by the Department of Health and Human Services or the EPA. The International Agency for Research on Cancer 94) categorized molybdenum trioxide as possibly carcinogenic to humans (Group 2B).

In healthy people, consumption of a diet high in molybdenum usually does not pose a health risk because the molybdenum is rapidly excreted in urine 95). One study assessed the effect of high dietary intakes of molybdenum (10–15 mg/day) in an area of Armenia where the soil contains very high levels of molybdenum 96). The affected individuals experienced achy joints, gout-like symptoms, and abnormally high blood levels of uric acid 97).

In 2005, a case study 98) was reported of an individual with high molybdenum exposure. An electrician with high occupational molybdenum exposure presented with hyperuricemia and gouty arthritis, which was ascribed to the molybdenum exposure 99). During an exposure-free period, his symptoms lessened, but then again worsened when he was once again exposed to high levels of environmental molybdenum. The authors noted that the association could be circumstantial.

In 2008, Meeker et al 100) reported an association between male infertility (impaired sperm motility) and blood molybdenum levels, based on volunteers attending infertility clinics. In a follow-up study published 2 years later, it was reported that circulating testosterone levels were inversely associated with blood molybdenum levels in the same study population 101).

Given the absence of human studies, the Food and Nutrition Board (FNB) at the National Academies of Sciences, Engineering, and Medicine 102) established Upper Intake Levels (ULs) for molybdenum for healthy individuals based on levels associated with impaired reproduction and fetal development in rats and mice.

Table 3. Tolerable Upper Intake Levels (ULs) for Molybdenum

Birth to 6 monthsNone established*None established*
7–12 monthsNone established*None established*
1–3 years300 mcg300 mcg
4–8 years600 mcg600 mcg
9–13 years1,100 mcg1,100 mcg
14–18 years1,700 mcg1,700 mcg1,700 mcg1,700 mcg
19+ years2,000 mcg2,000 mcg2,000 mcg2,000 mcg

Footnote: * Breast milk, formula, and food should be the only sources of molybdenum for infants.

[Source 103) ]

Human data: Mining and metallurgy workers chronically exposed to 60 to 600 mg molybdenum/m3 reported an increased incidence of nonspecific symptoms that included weakness, fatigue, headache, anorexia, and joint and muscle pain 104).

Immediately Dangerous to Life or Health Concentrations: 5,000 mg molybdenum/m3

The available toxicological data contain no evidence that an acute exposure to a high concentration of insoluble molybdenum compounds would impede escape or cause any irreversible health effects within 30 minutes. However, the revised Immediately Dangerous to Life or Health Concentrations for insoluble molybdenum compounds is 5,000 mg molybdenum/m3 based on being 500 times the Occupational Safety and Health Administration permissible exposure limit (legal limit in the United States for exposure of an employee to a chemical substance) of 10 mg molybdenum/m3 (500 is an assigned protection factor for respirators and was used arbitrarily during the Standards Completion Program for deciding when the “most protective” respirators should be used for particulates).

References   [ + ]