Ecological and toxicological effects of inorganic nitrogen pollution in aquatic ecosystems: A global assessment.

We provide a global assessment, with detailed multi-scale data, of the ecological and toxicological effects generated by inorganic nitrogen pollution in aquatic ecosystems. Our synthesis of the published scientific literature shows three major environmental problems: (1) it can increase the concentration of hydrogen ions in freshwater ecosystems without much acid-neutralizing capacity, resulting in acidification of those systems; (2) it can stimulate or enhance the development, maintenance and proliferation of primary producers, resulting in eutrophication of aquatic ecosystems; (3) it can reach toxic levels that impair the ability of aquatic animals to survive, grow and reproduce. Inorganic nitrogen pollution of ground and surface waters can also induce adverse effects on human health and economy. Because reductions in SO2 emissions have reduced the atmospheric deposition of H2SO4 across large portions of North America and Europe, while emissions of NOx have gone unchecked, HNO3 is now playing an increasing role in the acidification of freshwater ecosystems. This acidification process has caused several adverse effects on primary and secondary producers, with significant biotic impoverishments, particularly concerning invertebrates and fishes, in many atmospherically acidified lakes and streams. The cultural eutrophication of freshwater, estuarine, and coastal marine ecosystems can cause ecological and toxicological effects that are either directly or indirectly related to the proliferation of primary producers. Extensive kills of both invertebrates and fishes are probably the most dramatic manifestation of hypoxia (or anoxia) in eutrophic and hypereutrophic aquatic ecosystems with low water turnover rates. The decline in dissolved oxygen concentrations can also promote the formation of reduced compounds, such as hydrogen sulphide, resulting in higher adverse (toxic) effects on aquatic animals. Additionally, the occurrence of toxic algae can significantly contribute to the extensive kills of aquatic animals. Cyanobacteria, dinoflagellates and diatoms appear to be major responsible that may be stimulated by inorganic nitrogen pollution. Among the different inorganic nitrogenous compounds (NH4 ,N H3 ,N O2 , HNO2 ,N O3 ) that aquatic animals can take up directly from the ambient water, unionized ammonia is the most toxic, while ammonium and nitrate ions are the least toxic. In general, seawater animals seem to be more tolerant to the toxicity of inorganic nitrogenous compounds than freshwater animals, probably because of the ameliorating effect of water salinity (sodium, chloride, calcium and other ions) on the tolerance of aquatic animals. Ingested nitrites and nitrates from polluted drinking waters can induce methemoglobinemia in humans, particularly in young infants, by blocking the oxygen-carrying capacity of hemoglobin. Ingested nitrites and nitrates also have a potential role in developing cancers of the digestive tract through their contribution to the formation of nitrosamines. In addition, some scientific evidences suggest that ingested nitrites and nitrates might result in mutagenicity, teratogenicity and birth defects, contribute to the risks of non-Hodgkin's lymphoma and bladder and ovarian cancers, play a role in the etiology of insulin-dependent diabetes mellitus and in the development of thyroid hypertrophy, or cause spontaneous abortions and respiratory tract infections. Indirect health hazards can occur as a consequence of algal toxins, causing nausea, vomiting, diarrhoea, pneumonia, gastroenteritis, hepatoenteritis, muscular cramps, and several poisoning syndromes (paralytic shellfish poisoning, neurotoxic shellfish poisoning, amnesic shellfish poisoning). Other indirect health hazards can also come from the potential relationship between inorganic nitrogen pollution and human infectious diseases (malaria, cholera). Human sickness and death, extensive kills of aquatic animals, and other negative effects, can have elevated costs on human economy, with the recreation and tourism industry suffering the most important economic impacts, at least locally. It is concluded that levels of total nitrogen lower than 0.5–1.0 mg TN/L could prevent aquatic ecosystems (excluding those ecosystems with naturally high N levels) from developing acidification and eutrophication, at least by inorganic nitrogen pollution. Those relatively low TN levels could also protect aquatic animals against the toxicity of inorganic nitrogenous compounds since, in the absence of eutrophication, surface waters

Review article Ecological and toxicological effects of inorganic nitrogen pollution in aquatic ecosystems: A global assessment

Background Hemodialysis is a common but potentially hazardous procedure. From February 17 to 20, 1996, 116 of 130 patients (89 percent) at a dialysis center (dialysis center A) in Caruaru, Brazil, had visual disturbances, nausea, and vomiting associated with hemodialysis. By March 24, 26 of the patients had died of acute liver failure. Methods A case patient was defined as any patient undergoing dialysis at dialysis center A or Caruaru's other dialysis center (dialysis center B) during February 1996 who had acute liver failure. To determine the risk factors for and the source of the outbreak, we conducted a cohort study of the 130 patients at dialysis center A and the 47 patients at dialysis center B, reviewed the centers' water supplies, and collected water, patients' serum, and postmortem liver tissue for microcystin assays. Results One hundred one patients (all at dialysis center A) met the case definition, and 50 died. Affected patients who died were older than those who survived (median age, 47 vs. 3...

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Liver Failure and Death after Exposure to Microcystins at a Hemodialysis Center in Brazil

In late May, 2007, a drinking water crisis took place in Wuxi, Jiangsu Province, China, following a massive bloom of the toxin producing cyanobacteria Microcystis spp. in Lake Taihu, China’s third largest freshwater lake. Taihu was the city’s sole water supply, leaving approximately two million people without drinking water for at least a week. This cyanobacterial bloom event began two months earlier than previously documented for Microcystis blooms in Taihu. This was attributed to an unusually warm spring. The prevailing wind direction during this period caused the bloom to accumulate at the shoreline near the intake of the water plant. Water was diverted from the nearby Yangtze River in an effort to flush the lake of the bloom. However, this management action was counterproductive, because it produced a current which transported the bloom into the intake, exacerbating the drinking water contamination problem. The severity of this microcystin toxin containing bloom and the ensuing drinking water crisis were attributable to excessive nutrient enrichment; however, a multi-annual warming trend extended the bloom period and amplified its severity, and this was made worse by unanticipated negative impacts of water management. Long-term management must therefore consider both the human and climatic factors controlling these blooms and their impacts on water supply in this and other large lakes threatened by accelerating eutrophication.

A Drinking Water Crisis in Lake Taihu, China: Linkage to Climatic Variability and Lake Management

https://hal-univ-rennes1.archives-ouvertes.fr/hal-00875835/document

State of knowledge and concerns on cyanobacterial blooms and cyanotoxins.

Dam construction and associated flooding along rivers can alter ecosystems and pose serious threats to the welfare and health of local populations. This article describes a severe gastroenteritis epidemic in the Paulo Afonso region of Brazil's Bahia State related to flooding of the newly constructed Itaparica Dam's reservoir in 1988. Some 2,000 gastroenteritis cases, 88 of which resulted in death, were reported over a 42-day period. Responding to the outbreak, clinical data and water sample test results were reviewed; blood and fecal specimens from gastroenteritis patients were subjected to bacteriologic, virologic, and toxicologic testing; and drinking water samples were examined for microorganisms and heavy metals. The results revealed that the source of the outbreak was water impounded by the dam and pointed to toxin produced by cyanobacteria as the responsible agent. Proliferation of these microbes, present at concentrations of 1,104 to 9,755 standard cyanobacterial units per milliliter in untreated water, appears to have been encouraged by the decomposing biomass and other conditions prevailing in the newly flooded reservoir area.

Gastroenteritis epidemic in the area of the Itaparica Dam, Bahia, Brazil

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Gastroenteritis epidemic in the area of the Itaparica Dam, Bahia, Brazil