Mercury Hazards to Living Organisms - Chapter 8 pdf

CHAPTER 8 Lethal Effects of Mercury This chapter synthesizes available literature on the lethality of inorganic and organic mercury compounds to freshwater and marine biota; the effect o

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PART 3 Lethal and Sublethal Effects of Mercury

under Controlled Conditions

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CHAPTER 8 Lethal Effects of Mercury

This chapter synthesizes available literature on the lethality of inorganic and organic mercury compounds to freshwater and marine biota; the effect of route of administration of various mer-curials on the survival of representative species of waterfowl, passerines, raptors, and other avian groups; and the lethality of organomercury compounds to humans, small laboratory mammals, livestock, domestic cats and dogs, and various species of wildlife

Death is the only biological variable now measured that is considered irreversible by all investigators Nevertheless, time of death is modified by a host of physical, chemical, biological, metabolic, and behavioral variables, and it is unfortunate that some regulatory agencies still set mercury criteria to protect natural resources and human health on the basis of death — usually concentrations producing 50.0% mortality — and some variable uncertainty factor Mercury criteria for protection of natural resources and human health, as discussed in Chapter 12, should be based —

at a minimum — on the highest dose tested or highest tissue concentration found that does not produce death, impaired reproduction, inhibited growth, or disrupted well-being

8.1 AQUATIC ORGANISMS

Lethal concentrations of mercury salts ranged from less than 0.1 µg Hg/L to more than 200.0 µg/L

for representative sensitive species of marine and freshwater organisms (Table 8.1) The lower concentrations of less than 2.0 µg/L recorded were usually associated with early developmental

stages, long exposures, and flowthrough tests (Table 8.1) Among teleosts, females and larger fish were more resistant to lethal effects of mercury than were males and smaller fishes (Diamond et al., 1989) Among metals tested, mercury was the most toxic to aquatic organisms, and organomercury compounds showed the greatest biocidal potential (Eisler, 1981; Jayaprakash and Madhyastha, 1987) In general, mercury toxicity was higher at elevated temperatures (Armstrong, 1979), at reduced salinities for marine organisms (McKenney and Costlow, 1981), and in the presence of other metals such as zinc and lead (Parker, 1979) Salinity stress, for example, especially abnormally low salinities, reduced significantly the survival time of mercury-exposed isopod crustaceans (Jones, 1973), suggesting that species adapted to a fluctuating marine environment — typical of the intertidal zone — could be more vulnerable to the added stress of mercury than species inhabiting more uniformly stable environments

The marine ciliate protozoan Uronema marinum, with an LC50 (24 h) value of 6.0 µg/L, failed to

develop resistance to mercury over an 18-week period (Parker, 1979) However, another marine

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156 MERCURY HAZARDS TO LIVING ORGANISMS

Table 8.1 Lethality of Inorganic and Organic Mercury Compounds to Selected Species

of Aquatic Organisms Chemical Species, Ecosystem, Taxonomic

Group, Species, and Other Variables

Concentration (µµµµg Hg/L medium) Effect a Ref b

Inorganic Mercury: Freshwater

Crustaceans

Molluscs

Rainbow mussel, Villosa iris:

Juveniles; age 2 months; not fed during

exposure

Juveniles; age 2 months; not fed during

exposure

Fish

Zebrafish, Brachydanio rerio; embryo-larvae < 2.0 No deaths 16

Air-breathing catfish, Clarias batrachus; adults 507.0 LC50 (96 h) 18 Catfish, Clarias lazera:

Channel catfish, Ictalurus punctatus;

embryo-larva:

Largemouth bass, Micropterus salmoides;

embryo-larva:

Rainbow trout, Oncorhynchus mykiss:

Embryo-larva:

Amphibians

Blanchard’s cricket frog, Acris crepitans

Kentucky small-mouthed salamander,

Jefferson’s salamander, Ambystoma

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LETHAL EFFECTS OF MERCURY 157

Table 8.1 (continued) Lethality of Inorganic and Organic Mercury Compounds to Selected Species

of Aquatic Organisms

Chemical Species, Ecosystem, Taxonomic

Spotted salamander, Ambystoma maculatum;

embryo-larva

31.0 (25.0–37.0) LC50 (144–168 h) 27 Marbled salamander, Ambystoma opacum;

embryo-larva

103.0 (63.0–153.0) LC50 (120–144 h) 27 Small-mouthed salamander, Ambystoma

texanum

27.0 (21.0–33.0) LC50 (144–168 h) 27

Eastern green toad, Bufo debilis debilis;

embryo-larva

Fowler’s toad, Bufo woodhousei fowlerei:

Red-spotted toad, Bufo punctatus;

embryo-larva

Narrow-mouthed toad, Gastrophryne

Southern gray treefrog, Hyla chrysoscelis;

embryo-larva

Treefrogs, Hyla spp.; embryo-larva; 5 species 2.4–2.8 LC50 (72–96 h) 2, 27 Frog, Microhyla ornata; tadpoles:

Tadpoles:

Spring peeper, Pseudocris crucifer;

embryo-larva

Bullfrog, Rana catesbeina; embryo-larva 6.3 (4.9–8.1) LC50 (144–192 h) 27 Frog, Rana cyanophlyctis:

Pig frog, Rana grylio; embryo-larva 59.0 (32.0–109.0) LC50 (144–192 h) 27 River frog, Rana heckscheri:

Pickerel frog, Rana palustris; embryo-larva 5.1 (4.0–6.2) LC50 (144 h) 27

Northern leopard frog, Rana pipiens pipiens;

embryo-larva

Southern leopard frog, Rana sphenocephala;

tadpoles; fed diets containing various

concentrations of HgCl2 for 254 d:

28.0% dead in 240 d

34

South African clawed frog, Xenopus laevis;

tadpole

(continued)

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Inorganic Mercury: Marine

Protozoans

Coelenterates

Coral, Porites asteroides:

measured

180.0 (measured)

3 of 6 colonies dead in 72 h; remaining 3 colonies survived exposure for at least 15 d

25

Molluscs

Softshell clam, Mya arenaria:

Hardshell clam, Mercenaria mercenaria:

American oyster, Crassostrea virginica:

Mud snail, Nassarius obsoletus:

Slipper limpet, Crepidula fornicata:

Crustaceans

Mysid shrimp, Mysidopsis bahia:

Hermit crab, Pagurus longicarpus:

Prawn, Penaeus indicus:

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Annelids

Sandworm, Nereis virens:

Echinoderms

Starfish, Asterias rubens:

Fish

Tidewater silverside, Menidia peninsulae;

larvae, age 26 days

Mummichog, Fundulus heteroclitus:

Organic Mercury: Freshwater

Planarians

Flatworm, Dugesia dorotocephala:

Crustaceans

Fish

Rainbow trout:

Air-breathing catfish, Clarias batrachus;

adults:

(continued)

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ciliate protozoan, Uronema nigricans, acquired tolerance to mercury after feeding on

mercury-laden bacteria and subsequently exposed to increasing levels of mercury in solution (Berk et al.,

1978) The phenomenon of acquired mercury tolerance in U nigricans occurred in a single generation (Berk et al., 1978) Among coral colonies of Porites asteroides, the LC50 (72 h) value

was 180.0 µg Hg/L, as HgCl2 Death was preceded by polyp contraction during the first 8 h, color loss within 24 h, and tissue loss within 48 h (Bastidas and Garcia, 2004)

In general, salts of mercury and its organic compounds have been shown in short-term bioassays

to be more toxic to marine organisms than salts of other heavy metals (Kobayashi, 1971; Conner, 1972; Schneider, 1972; Berland et al., 1976; Reish et al., 1976; Eisler and Hennekey, 1977) To oyster embryos, for example, mercury salts were more toxic than salts of silver, copper, zinc, nickel, lead, cadmium, arsenic, chromium, manganese, or aluminum (Calabrese et al., 1973); to clam embryos, mercury was the most toxic metal tested, followed, in order, by silver, zinc, nickel, and

Amphibians

Organic Mercury: Marine

Molluscs

American oyster, Crassostrea virginica:

0–10 ° C to methylmercury or phenylmercury

Most moribund or dead 24

removed at day 19 and transferred to flowing mercury-free seawater

All dead within 14 days 24

Crustaceans

Fish

Mummichog, Fundulus heteroclitus:

Eggs, polluted creek (sediment content of

10.3 mg Hg/kg)

a Abbreviations: LT = lifetime exposure; h = hours; d = days; min = minutes.

b Reference: 1, USEPA, 1980; 2, Birge et al., 1979; 3, Verma and Tonk, 1983; 4, Parker, 1979; 5, Eisler and Hennekey, 1977; 6, USEPA, 1985; 7, Thain, 1984; 8, Nelson et al., 1976; 9, Gentile et al., 1983; 10, Glickstein, 1978; 11, McClurg, 1984; 12, Best et al., 1981; 13, Jayaprakash and Madhyastha, 1987; 14, Kanamadi and Saidapur, 1991; 15, Punzo, 1993; 16, Dave and Xiu, 1991; 17, Hilmy et al., 1987; 18, Kirubagaran and Joy, 1988; 19, Diamond et al., 1989; 20, Niimi and Kissoon, 1994; 21, Khan and Weis, 1987; 22, Hamasaki et al., 1995; 23, Mayer, 1987; 24, Cunningham and Tripp, 1973; 25, Bastidas and Garcia, 2004; 26, Shah and Altindag, 2004; 27, Birge et al., 2000; 28, Paulose, 1988; 29, Ghate and Mulherkar, 1980; 30, Rao and Madyastha, 1987;

31, Punzo, 1993; 32, De Zwart and Sloof, 1987; 33, Valenti et al., 2005; 34, Unrine et al., 2004.

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lead (Calabrese and Nelson, 1974) Glickstein (1978) reported an LC50 (48 h) value of 5.7 µg

Hg/L, as inorganic mercury, to embryos of the Pacific oyster, Crassostrea gigas; however, embryos

were relatively insensitive to mercury 24 h postfertilization, and survival was enhanced by a variety

of factors, including ambient selenium concentrations

Mercury toxicity to crustaceans was markedly influenced by developmental stage, diet, sex, salinity, tissue sensitivity, and selenium Larvae and newly molted crustaceans were more sensitive

to mercury toxicity than were adults of the same species (Wilson and Conner, 1971; Vernberg et al., 1974; Shealy and Sandifer, 1975) Starved larvae of the grass shrimp had lower survival rates than fed larvae when subjected to mercury insult (Shealy and Sandifer, 1975) Also, male adult fiddler

crabs (Uca pugilator) were more sensitive to mercury salts than females (Vernberg et al., 1974) Lethality of mercury salts to the porcelain crab (Petrolisthus armatus) were most pronounced at

lower salinities within the range of 7 to 35‰ (Roesijadi et al., 1974) A similar pattern was recorded

for the fiddler crab, Uca pugilator (Vernberg et al., 1974) Adult prawns (Leander serratus) held

in lethal solutions of mercury (50.0 mg inorganic Hg/L; 1.0 mg organic mercury/L) for 3 h contained

at death 320.0 to 460.0 mg Hg/kg DW in antennary gland (Corner and Rigler, 1958) High levels

of selenium (> 5.0 mg/L) increased mercury toxicity to larvae of dungeness crab, Cancer magister,

to levels below the LC50 (96 h) value of 6.6 µg Hg/L; however, moderate selenium values of 0.01

to 1.0 mg/L tended to decrease mercury toxicity (Glickstein, 1978)

Many acute toxicity bioassays were of 96-h duration, a duration that allows the senior investi-gator and technicians alike the opportunity to enjoy an uninterrupted weekend But it is clear from Table 8.1 that assays of 168-h duration produced LC50 values up to 45 times lower (more toxic) than did the 96-h assays, as was shown for mud snails It is recommended that acute toxicity bioassays with mercury and other toxicants and estuarine fauna should consist of a minimal 10-day continuous exposure followed by a 10-day observation period (Eisler, 1970)

Signs of acute mercury poisoning in fish, included flaring of gill covers, increased the frequency

of respiratory movements, loss of equilibrium, excessive mucous secretion, darkening of coloration, and sluggishness (Armstrong, 1979; Hilmy et al., 1987) Signs of chronic mercury poisoning included emaciation (due to appetite loss), brain lesions, cataracts, diminished response to change

in light intensity, inability to capture food, abnormal motor coordination, and various erratic behaviors (Armstrong, 1979; Hawryshyn et al., 1982) Total mercury concentrations in tissues of mercury-poisoned adult freshwater fish that died soon thereafter ranged (in mg/kg fresh weight) from 6.0 to 114.0 in liver, 3.0 to 42.0 in brain, 5.0 to 52.0 in muscle, and 3.0 to 35.0 in whole body (Armstrong, 1979; Wiener and Spry, 1996) Whole body concentrations up to 100.0 mg/kg FW

were reportedly not lethal to rainbow trout, Oncorhynchus mykiss, although 20.0 to 30.0 mg/kg

FW in that species were associated with reduced appetite, loss of equilibrium, and hyperplasia of

gill epithelium (Niimi and Lowe-Jinde, 1984) Brook trout, Salvelinus fontinalis, however, showed

toxic signs and death at whole body residues of only 5.0 to 7.0 mg/kg FW (Armstrong, 1979) Some fish populations have developed a resistance to methylmercury, but only in the gametes

and embryonic stage For example, eggs of the mummichog (Fundulus heteroclitus), an estuarine

cyprinodontiform fish, from a mercury-contaminated creek, when compared to a reference site, were more than twice as resistant to methylmercury (LC-50 values of 1.7 mg Hg/L vs 0.7 mg Hg/L) when exposed for 20 min prior to combination with untreated sperm Eggs from the polluted creek that were subjected to 1.0 or 2.5 mg CH3HgCl/L produced embryos with a 5.0 to 7.0% malformation frequency vs 32.0% malformations at 1.0 mg/L and little survival at 2.5 mg/L in

the reference group (Khan and Weis, 1987) Genetic polymorphism in mosquitofish (Gambusia

sp.) at specific enzyme loci are thought to control survival during mercury exposure (Diamond

et al., 1989) In one population of mosquitofish during acute exposure to mercury, genotypes at

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three loci were significantly related to survival time, as was heterozygosity However, neither genotype nor heterozygosity were related to survival in a different population of mosquitofish during acute mercury exposure (Diamond et al., 1991)

Embryo-larva tests with amphibians and inorganic mercury showed that 6 of the 21 species tested were more sensitive than rainbow trout embryo-larva tests and 15 were less sensitive; however, all 21 amphibian species were more sensitive than largemouth bass embryos (Birge et al., 2000; Table 8.1) Amphibian embryos were the most sensitive stage tested to mercury and other chemicals owing to the relatively high permeability of the egg capsule at this time (Birge et al., 2000) In general, organomercurials were 3 to 4 times more lethal than inorganic mercury com-pounds to amphibians when the same species and life stage were tested (Table 8.1)

Exposure pathways for adult amphibians include soils (dermal contact, liquid water uptake), water (dermal contact with surface water), air (cutaneous and lung absorption), and diet (adults are carnivores) All routes of exposure are affected by various physical, chemical, and other factors Dietary exposure in adults, for example, is related to season of year, activity rates, food availability, consumption rate, and assimilation rates (Birge et al., 2000) Knowledge of these modifiers is necessary for adequate risk assessment of mercury as a possible factor in declining amphibian populations worldwide

8.2 TERRESTRIAL INVERTEBRATES

Methylmercury compounds at concentrations of 25.0 mg Hg/kg in soil were fatal to all tiger worms

(Eisenia foetida) in 12 weeks; at 5.0 mg/kg, however, only 21.0% died in a similar period (Beyer

et al., 1985) Inorganic mercury compounds were also toxic to earthworms (Octochaetus pattoni);

in 60 days, 50.0% died at soil Hg2+ levels of 0.79 mg/kg, and all died at 5.0 mg/kg (Abbasi and Soni, 1983)

8.3 REPTILES

Data on mercury lethality in reptiles are scarce, and those available suggest that sensitivity may

be both species and age dependent (Rainwater et al., 2005) For example, juveniles of the corn

snake, Elaphe guttata, fed diets containing 12.0 mg methylmercury/kg FW diet all died within

days (Bazar et al., 2002) However, adults and offspring from treated adults of the garter snake,

Thamnophis sirtalis, fed diets containing up to 200.0 mg methylmercury/kg FW diet all survived

and showed no sign of toxicity (Wolfe et al., 1998)

8.4 BIRDS

Signs of mercury poisoning in birds include muscular incoordination, falling, slowness, fluffed feathers, calmness, withdrawal, hyporeactivity, hypoactivity, and eyelid drooping In acute oral

exposures, signs appeared as soon as 20 min post-administration in mallards, Anas platyrhynchos, and 2.5 h in ring-necked pheasants, Phasianus colchicus Deaths occurred between 4 and 48 h in

mallards and 2 and 6 days in pheasants; remission took up to 7 days (Hudson et al., 1984) In

studies with coturnix, Coturnix sp., Hill (1981) found that methylmercury was always more toxic

than inorganic mercury, and that young birds were usually more sensitive than older birds Fur-thermore, some birds poisoned by inorganic mercury recovered after treatment was withdrawn, but chicks that were fed methylmercury and later developed toxic signs usually died, even if treated feed was removed Coturnix subjected to inorganic mercury, regardless of route of administration, showed a violent neurological dysfunction that ended in death 2 to 6 h posttreatment The withdrawal

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syndrome in coturnix poisoned by Hg2+ was usually preceded by intermittent, nearly undetectable tremors, coupled with aggressiveness toward cohorts; time from onset to remission was usually 3

to 5 days, but sometimes extended to 7 days Coturnix poisoned by methylmercury appeared normal until 2 to 5 days posttreatment; then, ataxia and low body carriage with outstretched neck were often associated with walking In advanced stages, coturnix lost locomotor coordination and did not recover; in mild to moderate clinical signs, recovery usually took at least 1 week (Hill, 1981) Mercury toxicity to birds varies with the form of the element, dose, route of administration, species, sex, age, and physiological condition (Fimreite, 1979) For example, in northern bobwhite chicks fed diets containing methylmercury chloride, mortality was significantly lower when the solvent was acetone than when it was another carrier such as propylene glycol or corn oil (Spann

et al., 1986) In addition, organomercury compounds interact with elevated temperatures and pes-ticides, such as DDE and parathion, to produce additive or more-than-additive toxicity, and with selenium to produce less-than-additive toxicity (Fimreite, 1979) Acute oral toxicities of various mercury formulations ranged between 2.2 and about 31.0 mg Hg/kg body weight for most avian species tested (Table 8.2) Similar data for other routes of administration were 4.0 to 40.0 mg/kg for diet and 8.0 to 15.0 mg/kg body weight for intramuscular injection (Table 8.2)

Residues of mercury in experimentally poisoned passerine birds usually exceeded 20.0 mg/kg

FW, and were similar to concentrations reported in wild birds that died of mercury poisoning

(Finley et al 1979) In one study with the zebra finch (Poephila guttata), adults were fed

methyl-mercury in the diet for 76 days at dietary levels of < 0.02 (controls), 1.0, 2.5, or 5.0 mg Hg/kg

DW ration (Scheuhammer, 1988) There were no signs of mercury intoxication in any group except the high-dose group, which experienced 25.0% dead and 40.0% neurological impairment Dead birds from the high-dose group had 73.0 mg Hg/kg FW in liver, 65.0 in kidney, and 20.0 in brain; survivors without signs had 30.0 in liver, 36.0 in kidney, and 14.0 mg Hg/kg FW in brain; impaired birds had 43.0 mg Hg/kg FW in liver, 55.0 in kidney, and 20.0 in brain (Scheuhammer, 1988) Mercury levels in tissues of poisoned wild birds were highest (45.0 to 126.0 mg/kg FW) in

red-winged blackbirds (Agelaius phoeniceus), intermediate in European starlings (Sturnus vulgaris) and cowbirds (Molothrus ater), and lowest (21.0 to 54.0) in common grackles (Quiscalus quiscula).

In general, mercury residues were highest in the brain, followed by the liver, kidney, muscle, and carcass Some avian species are more sensitive than passerines (Solonen and Lodenius, 1984; Hamasaki et al., 1995) Liver residues (in mg Hg/kg FW) in birds experimentally killed by

methyl-mercury ranged from 17.0 in red-tailed hawks (Buto jamaicensis) to 70.0 in jackdaws (Corvus

monedula); values were intermediate in ring-necked pheasants, kestrels (Falco tinnunculus), and

black-billed magpies (Pica pica) (Solonen and Lodenius; Hamasaki et al., 1995) Experimentally poisoned grey herons (Ardea cinerea) seemed to be unusually resistant to mercury; lethal doses

produced residues of 415.0 to 752.0 mg Hg/kg dry weight of liver (Van der Molen et al., 1982) However, levels of this magnitude were frequently encountered in livers from grey herons collected during a massive die-off in the Netherlands during a cold spell in 1976; the interaction effects of cold stress, mercury loading, and poor physical condition of the herons are unknown (Van der Molen et al., 1982)

8.5 MAMMALS

Mercury is easily transformed into stable and highly toxic methylmercury by microorganisms and other vectors (De Lacerda and Salomons, 1998; Eisler, 2000) Methylmercury affects the central nervous system in humans — especially the sensory, visual, and auditory areas concerned with coordination; the most severe effects lead to widespread brain damage, resulting in mental derange-ment, coma, and death (Clarkson and Marsh, 1982; USPHS, 1994) Methylmercury has long residence times in aquatic biota and consumption of methylmercury-contaminated fish is implicated

in more than 150 deaths and more than 1000 birth defects in Minamata, Japan, between 1956 and

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