Reviews of Environmental Contamination and Toxicology

Risk from Acanthamoeba keratitis is complex, depending upon the virulence of the particular strain, exposure, trauma, or other stress to the eye, and host immune response. Bacterial endosymbionts may also play a factor in the pathogenicity of Acanthamoeba. Which factor(s) may be the most important is not clear. The ability of the host to produce IgA antibodies in tears may be a significant factor. The immune response of the host is a significant risk factor for GAE infection. If so, then a certain subpopulation with an inability to produce IgA in the tears may be at greatest risk. There was no sufficient data on the occurrence or types of Acanthamoeba in tapwater in the U.S. Published work on amoebal presence in tapwater does not provide information on the type of treatment the water received or the level of residual chlorine. Assessment of the pathogenicity by cell culture and molecular methods of Acanthamoeba in tapwater would also be useful in the risk assessment process for drinking water. The possibility that Acanthamoeba spp. might serve as vectors for bacterial infections from water sources also should be explored. The bacterial endosymbionts include an interesting array of pathogens such as Vibrio cholerae and Legionella pneumophila, both of which are well recognized waterborne/water-based pathogens. Work is needed to determine if control of Acanthamoeba spp. is needed to control water-based pathogens in water supplies.

Arsenic sources to the biosphere associated with gold mining include waste soil and rocks, residual water from ore concentrations, roasting of some types of gold-containing ores to remove sulfur and sulfur oxides, and bacterially enhanced leaching. Arsenic concentrations near gold mining operations are elevated in abiotic materials and biota: maximum total arsenic concentrations measured were 560 μg/L in surface waters, 5.16 mg/L in sediment pore waters, 5.6 mg/kg DW in bird liver, 27 mg/kg DW in terrestrial grasses, 50 mg/kg DW in soils, 79 mg/kg DW in aquatic plants, 103 mg/kg DW in bird diets, 225 mg/kg DW in soft parts of bivalve molluscs, 324 mg/L in mine drainage waters, 625 mg/kg DW in aquatic insects, 7,700 mg/kg DW in sediments, and 21,000 mg/kg DW in tailings.

Single oral doses of arsenicals that were fatal to 50% of tested species ranged from 17 to 48 mg/kg BW in birds and from 2.5 to 33 mg/kg BW in mammals. Susceptible species of mammals were adversely affected at chronic doses of 1–10 mg As/kg BW or 50 mg As/kg diet. Sensitive aquatic species were damaged at water concentrations of 19–48 μg As/L, 120 mg As/kg diet, or tissue residues (in the case of freshwater fish) >1.3 mg/kg fresh weight. Adverse effects to crops and vegetation were recorded at 3–28 mg of water-soluble As/L (equivalent to about 25–85 mg total As/kg soil) and at atmospheric concentrations >3.9 μg As/m³. Gold miners had a number of arsenic-associated health problems, including excess mortality from cancer of the lung, stomach, and respiratory tract. Miners and school children in the vicinity of gold mining activities had elevated urine arsenic of 25.7 μg/L (range, 2.2–106.0 μg/L). Of the total population at this location, 20% showed elevated urine arsenic concentrations associated with future adverse health effects; arsenic-contaminated drinking water is the probable causative factor of elevated arsenic in their urine. Proposed arsenic criteria to protect human health and natural resources are listed and discussed. Many of these proposed criteria do not adequately protect sensitive species.