Air Quality Criteria for Lead Volume II of II - (NEPIS)(EPA) - US ...

AX7.2.3 Aquatic Species Response/Mode of Action
Recent advancements in understanding the responses of aquatic biota to Pb exposure are
highlighted in this section. A summary of the conclusions on the review of aquatic responses to
Pb from the appropriate sections of the 1986 Lead AQCD, Volume II (U.S. Environmental
Protection Agency, 1986a) and the subsequent conclusions and recommendations contained in
the EPA staff review of that document (U.S. Environmental Protection Agency, 1990) are also
provided. In addition, this section summarizes research subsequent to the 1986 Lead AQCD on
Pb uptake into aquatic biota, effects of Pb speciation on uptake, resistance mechanisms to Pb
toxicity, physiological effects of Pb, factors that affect responses to Pb, and factors associated
with global climate change. Areas of research that are not addressed here include literature
related to exposure to Pb shot or pellets and studies that examine human health-related endpoints
(e.g., hypertension), which are described in other sections of this document.
AX7.2.3.1 Lead Uptake
Lead is nutritionally nonessential and non-beneficial and is toxic to living organisms in all
of its forms (Eisler, 2000). Lead can bioaccumulate in the tissues of aquatic organisms through
ingestion of food and water and adsorption from water (Vázquez et al., 1999; Vink, 2002) and
subsequently lead to adverse effects if tissue levels are sufficiently high (see Section AX7.2.5).
Recent research has suggested that due to the low solubility of Pb in water, dietary Pb (i.e., lead
adsorbed to sediment, particulate matter, and food) may contribute substantially to exposure and
toxicity in aquatic biota (Besser et al., 2005). Besser et al. (2004) exposed the amphipod
Hyalella azteca to concentrations of Pb to evaluate the influence of waterborne and dietary Pb
exposure on acute and chronic toxicity. The authors found that acute toxicity was unaffected by
dietary exposure but that dietary Pb exposure did contribute to chronic toxic effects (i.e.,
survival, growth, reproduction) in H. azteca. Field studies in areas affected by metal
contamination (i.e., Clark Fork River, MO; Coeur d’Alene, ID) (Woodward et al., 1994, 1995;
Farag et al., 1994) have also demonstrated the effects of dietary metals on rainbow trout.
However, there has been a debate on the importance of dietary exposure, as few controlled
laboratory studies have been able to replicate the effects observed in the field studies (Hodson
et al., 1978; Mount, 1994; Erikson, 2001). This may be due to differences in the availability of
Pb from the dietary sources used in laboratory studies, differences in speciation, and/or
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