Hi Gavin,
Yes it's clear that most of what we "know" is what we are told or what we read. AS it turns out, we only truly "know" something when we study and experience it for ourselves. If you think about it. most of us don't even "know" our own language. We just hear our parents mumbling from the time we're in the crib, simply repeat whet we hear them say. When we finally start uttering words it's really only because we start life out as parrots. It's only when we grow a bit and study English or Danish, or whatever, that we understand the how and why of what we say.
My opinion is that if I'm going to read what someone else says of a thing then it's best to read from someone who actually gets paid to study that same thing that I'm interested in. As I mentioned before, few people even bother trying to understand why ammonia, nitrite and nitrate are toxic or even what the mitigating factors could be. I encourage you to study a document such as:
Ecological and toxicological effects of inorganic nitrogen pollution in aquatic ecosystems: A global assessment a modern assessment of nitrogen pollution worldwide. Nitrogen poisoning due to agricultural use of fertilizers and the run-off, which infects the ground and surface waters, has been implicated in a wide variety of species decline such as amphibians (frogs, salamanders and so forth). You have to buy the article, which immediately puts people off. People don't mind spending money for rubbish such as pH Down, Phosphozorb and the like, but paying money for knowledge? No way, it's better to stumble around in the dark.
In any case, the article has a very good description of the toxic mechanisms. Lets start with ammonia.
The ionized ammonia (NH4+) and unionized ammonia (NH3) are interrelated through the chemical equilibrium NH4+-OH-?NH3·H2O?NH3+H2O
The relative concentrations of NH4+ and NH3 are basically dependent on the pH and temperature of the water: as values of pH and temperature tend to increase, the concentration of NH3 also increases but the concentration of NH4+ decreases. The concentration of total ammonia is the sum of NH4+ and NH3 concentrations, and it is total ammonia that is analytically measured in water samples.
From this basic description you can immediately tell for example that your fish, being in a high pH and high temperature environment are more susceptible to ammonia/ammonium poisoning than fish kept in more acidic and/or cooler conditions. This means that controlling ammonia buildup via water changes are critical in a Rift Lake Chiclid Tank. Lets hear some more:
Unionized ammonia is very toxic to aquatic animals, particularly to fish, whereas ionized ammonia is nontoxic or appreciably less toxic. Moreover, unionized ammonia can cause toxicity to Nitrosomonas and Nitrobacter bacteria, inhibiting the nitrification process. This inhibition can also result in increased accumulation of NH4+ (plus NH3) in the aquatic environment, intensifying the toxicity to bacteria and aquatic animals.
So what does that tell you about the lunatics who dump ammonia into their tanks thinking that this speeds up the cycling of the tank?
The toxic action of unionized ammonia on aquatic animals, particularly on fish, may be due to one or more of the following
causes
(1) damage to the gill epithelium causing asphyxiation;
(2) stimulation of glycolisis and suppression of Krebs cycle causing progressive acidosis and reduction in blood oxygen-carrying capacity;
(3) uncoupling oxidative phosphorylation causing inhibition of ATP production and depletion of ATP in the basilar region of the brain;
(4) disruption of blood vessels and osmoregulatory activity upsetting the liver and kidneys;
(5) repression of immune system increasing the susceptibility to bacterial and parasitic diseases. In addition, ammonium ions can contribute to ammonia toxicity by reducing internal Na+ to possibly fatally low levels
These negative physiological effects can result in reduced feeding activity, fecundity and survivorship, decreasing populations sizes of aquatic animals....On the basis of acute and chronic toxicity data, water quality
criteria, ranging 0.05–0.35mgNH3–N/L for short-termexposures
and 0.01–0.02 mg NH3–N/L for long-term exposures, have been
estimated and recommended to protect sensitive aquatic animals
OK, lets see what's said about Nitrite Toxicity(NO2):
The nitrite ion (NO2
-) and unionized nitrous acid (HNO2) are interrelated through the chemical equilibrium (NO2-)+(H+)?HNO2
The relative concentrations of (NO2-) and HNO2 are basically dependent on the pH of the water: as the value of pH tends to increase, the concentration of (NO2-) can also increase, but the concentration of HNO2 decreases. The HNO2
concentration is 4–5 orders of magnitude less than the (NO2-)
concentration within the pH range 7.5–8.5.
Both chemical species, nitrite ion and unionized nitrous acid, may contribute to the total toxicity of nitrite to aquatic animals. Furthermore, as in the case of unionized ammonia, HNO2 can cause toxicity to Nitrosomonas and Nitrobacter bacteria, inhibiting the nitrification process. This inhibition can also result in increased accumulation of (NO2-) (plus HNO2) in the aquatic environment, intensifying the toxicity to bacteria and aquatic animals. Nevertheless, because in aquatic ecosystems the (NO2-) concentration usually is much higher than the HNO2 concentration, nitrite ions are considered to be major responsible for nitrite toxicity to aquatic animals.
No surprises there. Lets see the mechanism:
The main toxic action of nitrite on aquatic animals, particularly on fish and crayfish, is due to the conversion of oxygen-carrying pigments to forms that are incapable of carrying oxygen, causing hypoxia and ultimately death. In fish, entry of nitrite into the red blood cells is associated with the oxidation of iron atoms (Fe2+?
Fe3+), functional hemoglobin being converted into methemoglobin that is unable to release oxygen to body tissues because of its high dissociation constant. Similarly, in crayfish, entry of nitrite into the blood plasma is associated with the oxidation of copper atoms (Cu1+?Cu2+), whereby functional hemocyanin is converted into methemocyanin that cannot bind reversibly to molecular oxygen. In addition, the following toxic effects of nitrite on fish and crayfish have been found:
(1) depletion of extracellular and intracellular Chloride (Cl-) levels causing severe electrolyte imbalance;
(2) depletion of intracellular K+ and elevation of extracellular K+ levels affecting membrane potentials, neurotransmission, skeletal muscle contractions, and heart function;
(3) formation of N-nitroso compounds that are mutagenic and carcinogenic;
(4) damage to mitochondria in liver cells causing tissue O2 shortage;
(5) repression of immune system decreasing the tolerance to bacterial and parasitic diseases. Among the different environmental factors that can affect nitrite toxicity to aquatic animals, the water chloride concentration seems to be the most important. Because, in the gills of fish and crayfish, nitrite ions enter via the same route as chloride ions by being competitive inhibitors of the active branchial chloride uptake mechanism, elevated Cl− concentrations in the ambient water may inhibit the (NO2-) uptake and thereby protect fish and crayfish against nitrite toxicity. Calcium (Ca2+) and seawater (probably because of the high concentration of chloride and other ions) also can significantly reduce nitrite toxicity to fish and crayfish...
On the basis of acute toxicity data, Alonso (2005) has recently estimated water quality criteria, ranging 0.08–0.35 mg
NO2–N/L, that may be adequate to protect sensitive aquatic animals, at least during short-term exposures.
OK, lets hear about Nitrate:
The nitrate ion (NO3−) does not form an unionized species in the aquatic environment (i.e., HNO3 is completely dissociated to H+ and (NO3-), and consequently nitrate toxicity to aquatic animals is due to nitrate ions. As in the case of nitrite, the main toxic action of nitrate on aquatic animals, particularly on fish and crayfish, seems to be the conversion of oxygen-carrying pigments (hemoglobin, hemocyanin) to forms that are incapable of carrying oxygen (methemoglobin, methemocyanin). In fact, before it becomes toxic, nitrate must be converted into nitrite under internal body conditions. Nevertheless, owing to the low branchial permeability to nitrate ions, the NO3 - uptake in aquatic animals is more limited than the NO2 - uptake, which contributes to the relatively low toxicity of nitrate. The toxicity of nitrate ions in aquatic ecosystems has been traditionally considered to be irrelevant, despite the fact that elevated nitrate concentrations can actually exceed values as high as 25 mg NO3-N/L in surface waters and 100 mg NO3-N/L in ground waters. Furthermore, several laboratory studies have shown
that a nitrate concentration of 10 mg NO3–N/L (USA federal maximum level for drinking water) can adversely affect, at least during long-term exposures, sensitive aquatic animals. Freshwater animals appear to be more sensitive to nitrate toxicity than seawater animals, owing to the likely ameliorating effect of water salinity. However, early developmental stages of some marine invertebrates, naturally well adapted to low nitrate concentrations, may be so sensitive to nitrate ions as freshwater animals despite the ameliorating effect of water salinity. Among the different taxonomic groups of freshwater invertebrates and fish that have been exposed to nitrate toxicity, certain caddisflies, amphipods, and salmonid fishes seem to be the most sensitive, exhibiting short-term safe levels (120-hour LC0.01) and no observed effect concentrations (30-day NOEC) lower than 5 mg NO3–N/L.
On the basis of toxicity data, the Canadian Council of Ministers of the Environment (2003) has recommended water quality criteria, ranging 2.9–3.6 mg NO3–N/L, to protect freshwater and marine life, and Camargo et al. (2005a) have recently
proposed a maximum level of 2 mg NO3–N/L for the protection of sensitive aquatic animals.
So here we see that nitrate itself isn't even toxic. Only when internal functions of the fish reduce it to Nitrite is the toxicity caused. Even so, we see that the fishes uptake of NO3 is nowhere near the uptake of NO2.
A lot of this data come from the Canadian Fisheries branch, and it was determined that certain caddisflies, amphipods, and salmonid fishes were the most sensitive, therefore, the suggest concentration maxima are to protect these species. But does this apply to the species we keep. It's difficult to find data specific to our hobby but I was able to find this report:
Studies on the toxicity of ammonia, nitrate and their mixtures to guppy fry. This is an old study, 1977, but the data is still valid. If you just read the abstract, you can see that the difference in toxicity between ammonia and nitrate was several orders of magnitude - and that was for the fry, not the adults. Well, wild type guppies are bulletproof anyway so it not fair to say that your species have the same resistance to nitrate as these. It's likely that yours fall somewhere between the two extremes.
Also, when you read the parameters such as 72-h lc50 199 and 1.26 mg L-1 -N, you've got to interpret them properly. The fish were placed in a properly controlled and aerated tank. The chemical were added and fish kill was counted after a certain amount of time. the 72-h means 72 hours, or 3 days. LC50 refers to the Lethal Concentration that caused 50% of the fish to die. The -N only refers to the Nitrogen component of the compound, so the concentration of the compound has be calculated based on the ratio of Nitrogen in that compound. So 199ppm NO3-N has to be multiplied by 4.4 in order to determine the concentration of NO3 in the water. That means at a concentration of 875ppm NO3, 50% of the fish died after 3 days. Compare this number to the 15-20ppm NO3 per week suggestion and you'll see that we are nowhere close to the toxicity levels for this species anyway.
Of course these are short term data, so one could easily argue; my dosing may not kill the fish outright, but may lower their life expectancy. This is a valid argument, but the only way to know for sure is to do it. Fish die for lots of reasons. Somewhere in the data of causal factors will be the effects of long term exposure to nitrogenous salts. My own data indicates a negligible effect long term at dosing levels up to 3 times these values. Comfort levels are unaffected as the fish breed quite regularly and the fry grow to adulthood if they are not eaten. Apart from traumatic causes such as jumping, predation, CO2 overdose and so forth I see no decline in longevity for species that I keep.
The dosing numbers that you propose are fine, but you need to get more plants. Much more.
Bubble rates are easy. Just turn the knurled knob of the needle valve and count. I assume you have a bubble counter or that the diffuser you are using is transparent enough to see the bubbles enter the chamber?
As far as the brightness of your tank, try not to compare the wattage numbers. They are not relevant in this size tank because your bulbs are probably 5 feet long and that's a lot of light. The only true measure of lighting is measurement of the incident energy using a PAR meter.
Cheers,