Introduction

Selenium, like sulfur, is widely present in the environment, albeit at usually low concentration.   Like sulfur it is mostly present in the environment at higher oxidation states, i.e. as selenites and selenates (+4 and +6 oxidation states respectively), rarely as selenides (-2 oxidation state). It is almost never found as the element (0 oxidation state), but it is often produced in that state in biological treatment processes.

Selenites and selenates are generally soluble in water, more so than sulfites and sulfates. As such they cannot easily be removed from water by precipitation. Selenites can form insoluble surface complexes with metal oxides such as ferric hydrous oxide and manganese hydroxide, and can therefore be removed that way. Elemental selenium can also be produced from selenites or selenates by using a reduction process, biological or otherwise. It is a solid and it is possible to remove it from water in that form. Because of their acute toxicity, selenides need to be handled with care, and if present can also form insoluble metal salts or, at low pH, be emitted as H2Se, a noxious and highly toxic gas.

Organo-selenium species are important in understanding selenium toxicity. There are a great number of these species. Basically, any organic species that contains sulfur has an equivalent that contains selenium. As an example, the substitution of oxygen by sulfur in the cyanate ion gives thiocyanate, and the substitution of sulfur by selenium gives selenocyanate (OCN-, SCN- and SeCN- respectively). Of particular interest is the substitution of sulfur by selenium in the two sulfur-bearing amino acids, cysteine and methionine, giving selenocysteine and selenomethionine. Methylseleninic acid (CH3SeO2H) is another organo-selenium species which has been detected in water treated by biological processes and which is biologically active.

Selenium Toxicity - An Overview

The issue of selenium toxicity is complex but reducing toxicity is the main objective behind the development and commercialization of the Tracer Se process.

In recent years a number of large-scale bird mortality incidents have been associated with selenium. Examples include birds feeding and nesting at the Kesterson Reservoir in the San Joaquin Valley, California, between 1983 and 1985, eared grebes at the Salton Sea, California, in 1992 and, again, eared grebes at the Great Salt Lake, Utah in 2011. While selenium has been associated with the die-offs, the mechanism involved so is not well understood.
 

Acute Toxicity

To help understand toxicity data such as LC50 (the concentration at which 50% of the test organism will die after a stated time), the US EPA (2021) uses five toxicity categories. We can use this system to characterize the acute toxicity of selenium for a few aquatic organisms, as shown in Table 1.

Table 1 - Acute toxicity of some selenium species

As can be seen in Table 1, selenium is more acutely toxic for species lower in the food chain such as C. dubia, D. magna and H. azteca than for salmonids such as O. mykiss, O. tshawytscha and O. kisutch. In cases where acute toxicity data is available for both selenites and selenates, selenites are generally more toxic than selenates. Given that selenates are the dominant form of selenium in the aerobic aquatic environment, one could conclude that selenium is only slightly to moderately acutely toxic for most fish species, but can be highly toxic for small crustaceans such as D. magna and C. dubia.
 

Chronic Toxicity

Chronic toxicity is a different issue. Quoting Beatty (2014), “since ambient Se concentrations rarely reach levels that result in acute effects, the more common situation resulting in Se toxicity occurs at much lower chronic exposures.” The literature on selenium chronic toxicity is vast and confusing. Here are some key points from the Beatty paper:

Bacteria, fungi, algae, and invertebrates are fairly tolerant to elevated Se concentrations, and the more important role these organisms play is in the rapid transformation and transfer of Se into the aquatic food web. However … there is a high degree of variability in the toxic effects on algae and invertebrate taxa based on water Se concentrations, suggesting that Se uptake is very different among species at a given water concentration. …

“Fish and bird species have the highest sensitivities to both Se-related embryo mortality and developmental deformity, although amphibians and reptiles may also be sensitive to Se. … Reproductive and non-reproductive toxic effects may be seen in fish from chronic Se exposure. Reproductive effects are those originating from the maternal transfer of Se, while non-reproductive effects refer to the direct toxic impacts Se may have on juveniles and adults. Both reproductive and non-reproductive effects result primarily from the dietary intake of Se. There is also evidence that waterborne Se can elicit non-reproductive effects albeit at higher aqueous concentrations. …

“Many of the sublethal effects of Se in fish are similar to those found in birds… The more sensitive chronic effects in birds are related to reproductive impairment.”

One of the difficulties in assessing the chronic toxicity of selenium is that its uptake by living organisms depends on its speciation. Most lab studies have been done using selenites or selenates as these chemicals can easily be purchased and dosed at controlled concentration in the water. The issue is that the concentration of selenium in the tissues of living organisms does not depend on the total concentration of selenium in the water, but rather on the concentration of the various selenium species. Besser (1993) calculated the bioconcentration factor[1] of selenium for three organisms depending on the selenium speciation. All experiments used a total concentration of 10 µg Se/L in the water, but the selenium speciation varied:

Table 2 - Bioconcentration factors

In the same paper, Besser also reported that the speed of selenium uptake by the organisms studied also varies with the selenium speciation, with selenomethionine uptake being much faster than selenite, and selenite uptake being faster than selenate.

A decade later, Amweg (2003) did another study that looked at the potential for bioaccumulation of various selenium species. In this case Amweg was looking at a process named Algal/bacterial selenium reduction (ABSR) where inorganic selenium is converted to elemental selenium by a combination of algae and bacteria and then is removed from the water. This process is not widely used nowadays but was considered for a time for treating agricultural waste water containing large concentrations of selenium.

Amweg’s study “was intended to monitor Se concentrations in invertebrates found in the ABSR system and assess the effect of ABSR treatment on Se bioavailability.”

Amweg found that while the treatment managed to reduce the total selenium in the water by 60%, the bioconcentration factor for two algae species was actually increased by an order of magnitude after treatment. Overall, “{r}esults indicate that Se within and discharged from the ABSR was more bioavailable than that in the untreated drain water, and that except in the algal bioaccumulation test, organisms accumulated more Se exposed to ABSR-treated water than if exposed to untreated water.” Amweg conclusions are damning for the ABSR process:

“We believe that production of organo-Se by microbial activity…, and reduction of selenate to selenite which is then accumulated by algae … and incorporated into algal selenoproteins, caused the increased Se bioavailability seen after ABSR treatment. Higher organisms generally accumulate Se through their diet … and this Se-rich algal biomass presumably served as a Se source for the other invertebrates of the ponds. … Increased Se bioavailability is inherent in the system design due to its dependence on microbial Se reduction. … {G}iven that organic Se forms are approximately 1000 more bioavailable than selenate …, the system would have to be extraordinarily effective to achieve less bioaccumulation from the effluent than from the influent. Hypothetically, if the influent contained entirely selenate and the effluent contained entirely organic Se, the system would have to achieve greater than a 99.9% reduction in total Se concentration in order to be judged a success by the criterion of less bioaccumulation from the effluent.”

An adage of modern toxicology is that “solely the dose determines that a thing is not a poison”[2]: there is a relationship between the concentration of a substance and its effect. What is important, however, is not the concentration in the environment, but the concentration in the tissues.

Selenium is only moderately acutely toxic in water, especially when present as selenate. Because of the widely different values for the bioconcentration factor of the various selenium species and the lack of information on the selenium speciation in most papers looking at chronic toxicity, its chronic toxicity is difficult to assess. For biological treatment at least, the question of bioavailability of the selenium in the treated water is highly relevant in assessing the performance of the treatment system.

Even neglecting the effect of selenium on the reproduction success, the well-publicized die-off events mentioned above are a good example of selenium toxicity. It is however likely that these die-offs are complex events caused by bioaccumulation of selenium through the food chain up to a point where the selenium concentration became high enough that it caused acute toxicity in the predators. It is also likely that many species have issues with reproduction success because of a similar chain of events, even if the selenium concentration in the tissues is not sufficient to cause acute toxicity.

Download To Continue Reading Full White Paper On Selenium Removal From Wastewater 

^[2] Paraphrased from Paracelsus’ “Alle Dinge sind Gift, und nichts ist ohne Gift, allein die Dosis macht dass ein Ding kein Gift ist”, which can also be translated to “All things are poison, and nothing is without poison, the dosage alone makes it so a thing is not a poison.”

^[1] The bioconcentration factor, or BCF, is the ratio of an element in the tissue to the concentration of the same element in water.