Experimental Studies of Molybdenum Physiology and Toxicity
Molybdenum trioxide, molybdenum disulfide and molybdates
Toxicity studies of molybdenum trioxide, ammonium and calcium molybdates and molybdenum disulfide were carried out with rats and guinea pigs by the U.S. Public Health Service [Fairhall, 1945] Molybdenum trioxide and the molybdates when fed in large daily doses of from 1200 to 6000 mg Mo/kg body weight invariably proved fatal. Fatalities were few at doses of 120 to 600 mg. There were no fatalities with molybdenum disulfide. The highest dose corresponds to 420g for a 70 kg human being. In inhalation experiments (5 mg Mo/cu. ft. air) molybdenum trioxide and ammonium dimolybdate were injurious but molybdenum disulfide was much less so. Fumes of molybdenum trioxide produced by arcing across molybdenum electrodes were less toxic than molybdenum trioxide powder apparently because the rate of solution of the fume is greater on account of its small particle size (1.55 um) than that of the powder (15.6 um). So the fume is rapidly dissolved in the lungs and carried away from the site of deposition. Molybdenum trioxide and the molybdates also produced toxic effects when administered orally and by intraperitoneal injection in large doses (400 to 800 mg/kg).
Fairhall, L. T., Dunn, R. C., Sharpless, N. E. and Pritchard, E. A., The Toxicity of Molybdenum, U. S. Public Health Service, Public Health Bulletin, 1945, 293.
In a series of tests with rats and rabbits it was found that calcium, strontium, and zinc molybdates were nontoxic with respect to oral administration, skin absorption and skin irritation, and except for calcium molybdate, eye irritation [Climax Molybdenum Test]. Ammonium molybdate was toxic by oral administration and was also an eye irritant.
Climax Molybdenum Co.Test by Scientific Associates and New Drug Institute.
Toxicity data on molybdenum compounds are summarised in the Table. The low toxicity of molybdenum compounds is obvious when compared with, for example, arsenic and chromium. Ammonium molybdate is slightly toxic and molybdenum disulfide is completely nontoxic. The only effect of massive doses of molybdenum disulfide in acute oral toxicity tests with rabbits was the occurrence of diarrhoea for 24 to 48 hours after dosing. With molybdenum disulfide there was no increase of molybdenum storage in the body. The low toxicity of molybdenum disulfide is due presumably to its chemical inertness and insolubility in body fluids and it has been approved as a lubricant for bakery oven chains by the U.S. Food and Drug Administration. It should, however, be noted that in rats sulfide enhances the toxicity of molybdenum so it cannot be assumed that soluble or more reactive molybdenum-sulfur compounds will be nontoxic.
Acute Toxicities of Molybdenum Compounds towards Animals
| LD50/mg/l (mg/kg) |
||||
| Compound |
Animal |
oral |
Intra-peritoneal |
Ref. |
| MoO3 c |
guinea pig |
LD75 400 |
|
[1,2] |
| |
rat |
LD50190 |
|
[1,2] |
| MoO3 (pure) |
rat |
LD50 273 |
|
[3] |
| |
|
LD50 296-352 |
|
[4] |
| MoO3 (technical) |
rat |
LD50 666 |
|
[5] |
| Ammonium molybdate d |
guinea pig |
LD 2200 |
LD100 800 |
[1,2] |
| |
rat |
|
MLD 203 |
[1,2] |
| |
rabbit |
LD 1870 |
|
[1,2] |
| |
cat |
LD1600-3200 |
|
[1,2] |
| Sodium molybdate |
rat |
MLD 290 |
|
[1,2] |
| |
|
LD 671 |
|
|
| |
|
LD50 503 |
|
|
| |
dog |
|
LD 3200 |
|
| |
cat |
|
LD1600-3200 |
|
| |
|
|
LD50 344 |
[6] |
| Molybdate aq solution e |
chicken |
|
LD100 517+/-83 |
[7] |
| |
dog |
|
LD1001372+/-441 |
|
| |
pigeon |
|
LD100 607+/-119 |
|
| |
rat |
|
LD100 413+/-106 |
|
| Mo(VI) |
rat |
|
MLD 223 |
[8] |
| Mo(V) + glucose |
rat |
|
MLD 132 |
[8] |
| Mo(V ) + ascorbic acid |
rat |
|
MLD 1999 |
[8] |
| MoS2 |
rat |
|
LD50 > 15 000 |
[9] |
Notes and references
a The definition of toxicity is according to the U.S. Federal Hazardous Substances Labelling Act. The toxicity of the molybdenum compounds listed as toxic is "slight" (e.g., compare sodium arsenate, MLD10 for the rat by intraperitoneal injections). Abbreviations: LD, lethal dose for one animal; LDn, dose killing n% of a group of test animals; MLD, minimum lethal dose, i.e., the smallest of a number of doses which killed one or a group of test animals, all in mg/kg body weight.
b In tests of toxicity by skin absorption, skin irritation, and eye irritation (Test carried out for Climax Molybdenum Co. by Scientific Associates and New Drug Institute) the compounds listed were nontoxic except that ammonium and calcium molybdates were slight eye irritants.
c Some reports of high toxicity of MoO3 are based on the results of long term feeding studies wrongly presented as acute single dose studies
(e.g. LD50 125 mg/kg from L. Fairhall, R. Dunn, N. Sharpless, E. Pritchard, The toxicity of molybdenum, US Public Health Bulletin 293, 1945) (G.G. van Riper and J.C. Gilliland , ULLMANN’S ENCYCLOPEDIA OF INDUSTRIAL CHEMISTRY, 1990, A16, Ch. 12 )
d The description "ammonium molybdate" includes the compounds (NH4)2MoO4, (NH4)2Mo2O7 and (NH4)6Mo7O24.4H2O. There is unlikely to be any difference in the behaviour of the various molybdates.
e After a 60 min intravenous infusion.
[1] Saunders, W. B., Handbook of Toxicology, 1956, London.
[2] Fairhall, L. T., Dunn, R. C., Sharpless, N. E. and E. A. Pritchard, The Toxicity of Molybdenum, U.S. Public Health Service, Public Health Bulletin, 1945, 293
[3] Acute oral LD50 assay in rats FDRL-ID:81-0393 for AMAX Inc. Aug. 1981
[4] Food and Drug Research Laboratories Inc. Acute oral LD50 assay in rats for molybdenum trioxide pure grade, 1981, Waverly New York.
[5] Acute oral LD50 assay in rats FDRL-ID:81-0394 for AMAX Inc. Aug. 1981
[6] Irving Sax, N., Dangerous Properties of Industrial Materials, 1984, 6th Ed. Van Nostrand Reinhold Co. New York, 1953.
[7] Caujolle, F. and Changh, P. H., Agressologie, 1967, 8, 265 (Quoted in Lener, J. and Bibr, B., J. Hygiene, Epidemiology, Microbiology and Immunology, 1984, 28, 405).
[8] Lener, J. and Bibr, B., Proc. Int. Conf.: Heavy Metals in the Environment. Amsterdam 1981, 462. (Quoted in Lener, J. and Bibr, B., J. Hygiene, Epidemiology, Microbiology and Immunology, 1984, 28, 405).
[9] Acute oral LD50 assay in rats of MoS2 FDRL-ID 9589A for AMAX Inc. Nov 29 1987.
Inhalation of dusts of molybdenum trioxide
Inhalation of dusts of molybdenum trioxide (Table below) and the more soluble molybdates produced toxic effects. [Fairhall, 1945] The toxic effect of molybdenum trioxide dust was aggravated by silica [Mogilevskaya, 1961]. Precautions should be taken against the inhalation of dusts of molybdenum trioxide and the more soluble molybdates; maximum permissible concentrations in air recommended by the American Industrial Hygiene Association are 5 mg Mo/m3 (cf. Be, 0.002; V, 0.5; arsine, 0.3) over an eight-hour period. The World Health Organisation recommended in 1969 a "safe concentration zone" of molybdenum as 4-5 mg/m3.
Fairhall, L. T., Dunn, R. C., Sharpless, N. E. and Pritchard, E. A., The Toxicity of Molybdenum, U. S. Public Health Service, Public Health Bulletin, 1945, 293.
Mogilevskaya, O. Ya., Gig. Sanit., 1961, 26, 18.
| Observable |
Mice, male |
Mice, female |
Rats, male |
Rats, female |
| Survival |
0 |
0 |
0 |
0 |
| Mean body weights |
0 |
0 |
0 |
0 |
| Blood Mo (b) |
+ |
+ |
+ |
+ |
| Mo toxicity symptoms (c) |
0 |
0 |
0 |
0 |
| Bone density or curvature |
0 |
0 |
0 |
0 |
| Nasal and larynx lesions |
+ |
+ |
+ |
+ |
| Chronic inflammation in lungs |
0 |
0 |
+(d) |
+(d) |
| Lung carcinoma |
+ |
+ |
0?(e) |
0 (e) |
(a) Groups of 50 male and 50 femaleF344/N rats and B6C3F1 mice were exposed to MoO3 by inhalation at 0, 10, 30, or 100 mg/m3, 6 h/day, 5 days/week, for 2 years. Controls were not exposed. Plus (+) means a positive effect compared with the controls which increases with the level of exposure. Zero (0) means no effect.
(b) Mo concentrations (mg/g): male mice <0.10 (no MoO3) to 0.77 (highest MoO3), female mice 0.04 to 0.52, male rats 0.22 to 6.0, female rats,0.06 to 2.4
(c) e.g. diarrhoea, alopecia, dermatosis, anaemia.
(d) At highest exposures.
(e) For 1/50 animals.
Chan, P.C., Herbert, R.A., Roycroft, J.H., Haseman, J.K., Grumbein, S.L., Miller, R.A., Chou, B.J., Lung tumor induction by inhalation exposure to molybdenum trioxide in rats and mice, Toxicological Sciences, 1998, 45, 58-65.
Molybdenum trioxide inhalation studies in male rats
The following is a detailed summary of a recent study by K. Ozaki et al.
Correlations between non-neoplastic chronic pulmonary lesions and adrenal pheochromocytoma in 9 recent NTP, 2 year particulate inhalation studies in male F344 rats have been investigated. The re-evaluation of other lesions revealed significant associations of pheochromocytoma only with the severity of inflammation and fibrosis. The particulates investigated were all metal compounds and included molybdenum trioxide.
Pheochromocytomas are benign or malignant tumours which give a yellow-brown colour when stained with chromates. These tumours arise as a result of the increased production of catecholamines, such as dopamine, epinephrine and norepinephrine (adrenaline and noradrenaline) in the adrenal medulla in response to a stress which can be an environmental insult. (Catecholamines are synthesised in chromaffin cells.)
Generally exogenous agents that induce adrenal medullary neoplasia do not cause DNA damage so a carcinogenic response is due to an indirect mechanism.
Mammalian tissues are primarily aerobic and hence dependent upon a continuous supply of oxygen. Inadequate O2 delivery results in hypoxemia. Reduction in arterial O2 tension leads to the release of dopamine and other catecholamines. Activity of tyrosine hydroxlyase, the rate limiting step in the biosynthesis of catecholamines is enhanced in the carotid body and the adrenal gland during hypoxemia.
The hypothesis is that the area of lung tissue damaged by the inhalation of certain particulates is correlated positively with the degree of hypoxemia which leads to the pathological increase in tyrosine hydroxylase activity and the production of catecholamines.
The results of the studies relating to MoO3 are given in the following Table.
Results from the re-evaluation of 9 inhalation studies of the particulate compound MoO3 as reported by NTP.
| Dose |
Control 0 mg m-3 |
Low 10 mg m-3 |
Mid 30 mg m-3 |
High 100 mg m-3 |
| Lung |
|
|
|
|
| Proteinosis |
0/50 |
0/50 |
0/50 |
0/50 |
| Fibrosis, interstitium |
5/50 2.0 |
4/50 1.0 |
7/50 1.0 |
45/50 1.8 |
| Inflammation, chronic active |
10/50 1.8 |
7/50 1.6 |
37/50 1.2 |
48/50 2.1 |
| Alveolar epithelium hyperplasia |
12/50 1.8 |
14/50 1.6 |
16/50 1.2 |
7/50 1.3 |
| Metaplasia, squamous epithelium |
2/50 1.0 |
0/50 |
2/50 1.0 |
27/50 1.1 |
| Histiocytosis Increase in cells associated with inflammation |
11/50 1.9 |
13/50 1.3 |
35/50 1.3 |
46/50 1.7 |
| Alveolar/bronchial adenoma |
0/50 |
0/50 |
0/50 |
3/50 |
| Alveolar/bronchial carcinoma |
0/50 |
1/50 |
1/50 |
1/50 |
| Adrenal Medulla |
|
|
|
|
| Pheochromocytoma Benign + malignant |
15/50 |
13/50 |
18/50 |
18/50 |
| Hyperplasia |
32/50 2.1 |
27/50 2.1 |
28/50 2.1 |
29/50 2.5 |
Second number in each cell indicate the mean grade of severity
0 no involvement
1 min. up to 5 small lesions 10% of area
2 mild 10 - 25 % of area
3 moderate 26 - 50% of area
4 marked 51 - 75% of area
5 severe > 75% of area.
Terms used in the Table:
Proteinosis: Aggregates of homogeneous to granular material which stains with eosin within alveolar lumina.
Fibrosis: Dense fibrous tissue - thickening and scaring of connective tissue. This is considered secondary to inflammation.
Hyperplasia: Enlargement of an organ or tissue arising from the increased production of cells. In the case of the adrenal medulla in this study this is related to the increase in the production of catecholamines.
Metaplasia: Abnormal change in tissue.
Histiocytosis: Accumulation of alveolar macrophages with foamy cytoplasm and occasional multinucleated giant cells but few neutrophils. (Macrophages and neutrophils are associated with inflammation).
Adenoma: A gland-like benign tumour.
Carcinoma: A cancer.
Evaluation
General: In the controls inflammation with a smaller contribution from fibrosis was associated significantly (p<0.01) with the occurrence of pheochromocytomas.
None of the other non-neoplastic lung lesions were significantly correlated with the incidence of adrenal pheochromocytomas.
Molybdenum trioxide showed no dose related increase in pheochromocytoma incidence but the correlation between the incidence of pheochromocytoma and the severities of fibrosis and inflammation was highly significant (p < 0.01) and the strongest correlation was with inflammation.
Molybdenum trioxide showed one of the strongest correlations with inflammation of most test compounds. However, it was not understood why the increase in the incidence of pheochromocytomas did not follow the treatment-related increase in the severity of inflammation and fibrosis.
Pheochromocytomas can also be related to aging or in response to a wide variety of xenobiotic agents BUT these lesions are rare in humans and other animal species. They occur more frequently in male than female rats.
Ozaki, K., Haseman, J. K., Hailey, J. R., Maronpot, R. R., and Nyska, A., Association of adrenal pheochromocytoma and lung pathology in inhalation studies with particulate compounds in the male F344 rat - The national toxicology program experience, Toxicologic Pathology, 2002, 30, 263-270.
International Molybdenum Association toxicity testing programme
| Substance |
LD50 or LC50/ mg/l |
||
| |
Acute orala |
Acute inhalationb |
Acute dermalc |
| |
LD50 rats |
LC50 rats |
LD50 rats |
| Molybdenum trioxide (pure) |
3260 |
> 5.84 |
> 2000 |
| Molybdenum trioxide (tech) |
> 5000 |
> 3.93 |
> 2000 |
| Ammonium dimolybdate |
3883 |
> 2.08 |
> 2000 |
| Sodium molybdate |
4233 |
> 1.93 |
> 2000 |
| Molybdenum disulfide |
>2000 |
> 2.82 |
> 2000 |
| Risk phrase required if:d |
<2000 |
< 5 |
< 2000 |
Notes
a Acute oral is representative of relative toxicity by ingestion. Various doses were administered to rats (10/dose) by infusion into the stomach. Animals were observed for 14 days. For pure molybdenum trioxide there was a statistically significant difference between the oral LD50 in male and female rats: (male, 2689; female, 3830 mg/kg). The value given above is an average and is likely a low estimate.
b Acute inhalation is representative of relative toxicity by inhalation. Dust administered to rats (10) for 4 hours. Animals observed for 14 days.
c Acute dermal is representative of relative toxicity due to skin absorption. Various concentrations adminstered topically to rats (10). Animals observed for 14 days.
Skin irritation: Material applied to rabbit (6) skin for 4 hours. Animals observed for erythema and oedema daily for 4 days.
Eye irritation: Material applied to rabbit (6) eyes (100 mg). Animals observed for 7 days.
Skin sensitization: Guinea pigs exposed to material intradermally and topically twice (induction and challenge).
d All acute oral and dermal results were well above the level that requires a harmful classification and precautionary labelling. In the case of inhalation, in some cases it was not possible to generate a dust cloud of 5 mg/l. However, even at the highest concentrations generated there were no animal deaths and there is no basis to assume that labelling of these materials is indicated.
Toxicity studies on MoS2
Acute inhalation study in rats
The inhalation hazard associated with acute exposure to MoS2 is low.
The LC50 (4 hour) of MoS2 is > 2.82 mg/l in air.
Labelling of MoS2 with the risk phrase R20 Harmful by inhalation is not indicated.
MoS2 was administered as a particulate aerosol at a concentration of 2.82 mg/l of air for 4 h. The rats were observed for 14 d post exposure.
There were no deaths. No clinical signs and no changes of bodyweight compared with controls. Food and water consumption was similar to that of controls.
The ratio lung/body weight was similar to the ratio found for controls.
A grey appearance of the lungs was noted for all rats post mortem.
Acute oral toxicity to the rat
The acute lethal oral dose to rats of molybdenum disulphide was demonstrated to be greater than 2000 mg/kg bodyweight.
Molybdenum disulphide will not require labelling with the risk phrase R22, "Harmful if swallowed", in accordance with Commission Directive 93/2 I/EEC.
A group of ten fasted rats (five males and five females) received a single oral gavage dose of MoS2 formulated in 1% w/v aqueous methylcellulose and administered at a dose level of 2000 mg/kg bodyweight.
There were no deaths. Clinical signs of reaction to treatment in the main study, comprised piloerection, hunched posture and ungroomed appearance observed in all rats. There were no other clinical signs and recovery was complete in all instances by Day 4.
All rats were considered to have achieved satisfactory bodyweight gains throughout the study.
All animals were killed and examined macroscopically on Day 15, the end of the observation period. This examination revealed no abnormalities.
Eye irritation to rabbits
Molybdenum disulfide is not irritating to the eyes.
100 mg of MoS2 was instilled into the eyes of three rabbits. The animals were observed for three days. The MoS2 caused very slight conjunctaval irritation.
Acute dermal toxicity to the rat
Molybdenum disulfide will not require labelling with the risk phrase R21 (EU Commission Directive 93/21/EEC: ‘Harmful in contact with skin.’
The acute lethal dermal dose to rats of MoS2 > 2000 mg/kg bodyweight.
Ten rats received a topical application of MoS2 in 1% w/v aqueous methylcelulose, 2000mg/kg bodyweight.
There was no systemic response to MoS2 .
Four rats showed some dermal irritation which had disappeared 4 d after exposue was stopped.
Skin sensitisation in the guinea-pig
Molybdenum disulphide did not produce evidence of skin sensitisation (delayed contact hypersensitivity) in any of the ten test animals.
Molybdenum disulphide does not require labelling with the risk phrase R43 "May cause sensitisation by skin contact in accordance with Commission Directive 93/21/EEC.
The following dose levels were selected:
Intradermal injection:
10% w/v in Alembicol D
Topical application:
70% w/v in Alembicol D
Challenge application:
70 and 35% w1/v in Alembicol D
Ten test and five control guinea-pigs were used in this study.
Skin irritation to the rabbit
No dermal reactions were observed following a single, semi-occlusive application of molybdenurn disulphide to intact rabbit skin for four hours.
Molybdenum disulphide will not require labelling with the risk phrase R38 ‘Irritating to skin', in accordance with Commission Directive 93/21 /EEC.
Three rabbits were each administered a single dermal dose of 0.5 g of MoS2 and observed for four days.
Huntingdon Life Sciences Ltd Research Laboratory March 1998
Molybdenum metal and metal powder
As with other fine powders inhalation of quantities of molybdenum dust can be dangerous. Safety precautions have been described [Lamprey and Ripley, 1962]. Molybdenum metal as such and in alloys is not toxic and has been incorporated in stainless steels used in bone and joint surgery where resistance to corrosion by body fluids is required [Bechtol et al., 1959]. Molybdenum alloyed with cobalt and chromium has been used for some 40 years for surgical implants, dental prostheses etc. As with the stainless steel, molybdenum confers corrosion resistance.
Lamprey H. and Ripley, R. L., J. of the Electrochemical Soc., 1962, 109, 713.
Bechtol, C. O., Ferguson, B. and Laing, P. G., Metals and Engineering in Bone and Joint Surgery, The Williams and Wilkins Co., Baltimore, 1959.
Workers handling metals in welding and steelmaking are expected to have higher levels of trace metals. Interpretation of levels requires some knowledge of the toxicokinetics of a metal and the preferred medium for analysis for each: serum, whole blood or urine (preferably a 24-hour collection). Trends are often more informative than concentrations at one time. Molybdenum and vanadium are often found to be elevated among workers exposed to metals who show no evidence of clinical illness. The Mo level in the general population not occupationally exposed to Mo (the whole blood Mo reference range) is 5 - 50 nmol/l as used by the Trace Element and Environmental Toxicology Laboratory at the University of Alberta Hospitals. Mo is described as having 'very low toxicity' [Guidotti et al., 1997.]
Guidotti, T.L., Audette, R.J., Martin, C.J., Interpretation of the trace metal analysis profile for patients occupationally exposed to metals, Occupational Medicine-Oxford, 1997, 47 , 497-503.
Molybdenum carbide and silicide
Aqueous suspensions of MoC and MoSi2 administered intraperitoneally to mice in doses of 3000 mg/kg did not cause death [Chem. Abs., 1969]. Intratracheal administration of suspensions of these compounds to rats in doses of 50 mg/animal had pathological effects derived from the fibrogenic nature of the compounds. Maximum permissible concentrations in air are recommended as 6 mg Mo/m3
Chem. Abs., 1969, 71, 68977v.
Brakhnova, I. T. and Samsonov, G. V., Gig. Sanit., 1970, 35, 42.
Molybdenum pentachloride
Molybdenum pentachloride has a marked irritant effect on the tissues of rats [Spiridonova and Surorov, 1967]. The toxicity is due to hydrochloric acid produced during hydrolysis of the compound and not to molybdenum. Molybdenum pentachloride is a hazardous chemical and, if proper precautions are not taken, its industrial use involves danger of acute intoxication. There were no health problems in the production of MoCl5 at the former Climax Langeloth refinery and the Ann Arbor Laboratory.
Spiridonova, V. S. and Suvorov, S. V., Gig. Sanit., 1967, 32, 79.
Molybdenum pentachloride should be considered as a non-immunotoxic and a weak, nonspecific contact irritant. Immunotoxicity was studied in sheep by a 14 day subchronic exposure to MoCl5 at 1- 100 ppm in food. Contact hypersensitivity was determined by topical ear exposure to MoCl5 [Abdouh et al., 1995].
Abdouh, M., Krzystyniak, K., Flipo, D., Therien, H.M., Fournier, M., Cytometric Profile Of Molybdenum-Induced Contact Sensitization Versus A Strong Allergen Reaction To Oxazolone In Murine Auricular Lymph-Node (Aln) Test, International Journal Of Immunopharmacology, 1995, 17, 545-554.
Molybdenum hexacarbonyl and organomolybdenum compounds
Molybdenum hexacarbonyl is a solid which may be handled in the laboratory without special precautions. It is less toxic than the more volatile iron and nickel carbonyls. However, little is known about the toxic effects of molybdenum hexacarbonyl and organomolybdenum compounds [Vignoli and Defretin, 1963] and it is wise to assume that they are likely to be more toxic than MoO3 and molybdates and they should be handled in such a way that there is no danger of absorption through the skin or inhalation of their dusts and vapours.
Vignoli, L. and Defretin, J. P., Biologie medicale, 1963, 52, 319.
Volatile Mo(CO)6 and W(CO)6 are present in landfill gas from three different municipal waste deposits in concentrations of about 0.2-0.3 microg of Mo/m3 and 0.005-0.01 microg of W/m3. The chemical reactions which give rise to these carbonyls under landfill site conditions are not known. Because volatile metal carbonyls are toxic, questions about the occupational health of workers on landfills needs to be addressed [Feldmann and Cullen, 1997].
Feldmann, J., Cullen, W.R..,Occurrence of volatile transition metal compounds in landfill gas: Synthesis of molybdenum and Tungsten carbonyls in the environment, Environmental Science & Technology, 1997, 31, 2125-2129.
Comparative effects of molybdenum and other elements
In comparative toxicity studies with rats and mice sodium molybdate (LD50 1.45 m mol/kg body weight) was less toxic than sodium tungstate, sodium chromate and sodium vanadate [Pham Huu Chanh, 1965]. The irritant effect of sodium molybdate on skin, mucous membranes, and eyes was much smaller than that of sodium dichromate (an extreme irritant) [Climax Molybdenum Test].
Pham-Huu-Chanh, Arch. Intern. Pharmacodyn., 1965, 154, 243.
The ecotoxicological effects expressed as effect on respiratory rate and chlorophyll a content of the freshwater, alga Scenedesmus quadricauda and the bioaccumulation of six ions (Cu2+, Cu+, MoO42-, Mn2+, VO43-, Ni2+) and their associations were determined in comparison with a control [Fargasova, 1998]. The ion concentrations were equal to their EC50 concentrations: for Mo, ammonium heptamolybdate at 2.5 mg l-1. The pH’s of the solutions were not reported. Molybdate had no effect on the respiratory rate; the other ions caused the rate to increase. Combination of moybdate with nickel and copper decreased the rate (but not with manganese). Molybdate and the other ions caused the content of chlorophyll a to decrease. Bioaccumulation of molybdate was negligible MoO42- (< 0.2 %). Molybdate greatly decreased the uptake of Mn, Ni and Cu although these ions had no effect on the uptake of Mo.