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# Ecological Toxicity Information

Toxicity Profiles: a brief discussion of the general fate and transport processes associated with selected groups of COPECs.



## INORGANICS
Heavy metals and other inorganic compounds are naturally-occurring in the environment, and in some cases are essential nutrients (i.e., calcium, magnesium, potassium, and sodium). Inorganics tend to ad sorb strongly to clays, muds, humic, and organic materials. However, inorganics are very mobile in the environment. Depending upon the pH, hardness, salinity, oxidation state of the element, soil satura tion, and other factor s, inorganics are readily soluble.

Aluminum Toxicity information about aluminum is generally lacking. It has been determined that fish tend to be more sensitive to aluminum toxicity than aquatic invertebrates (Sparling et al. 1997 ). Aluminum can cause pulmonary an d developmental problems. Aluminum toxicity has been linked to soil pH--the amount of soluble aluminum, rather than the total aluminum concentration in the soil. Soil s at a site with a pH greater than 5.5 can generally be considered non-toxic in terms of aluminum.

Arsenic In plants, arsenic has been shown to cause wilting, chlorosis, browning, dehydration, mortality, and inhi bition of light ac tivation (Eisler 1988a ). Arsenic is a carcinogen (cancer-causing), teratogen, and possible mu tagen (causing mutations in genes/DNA) in mammals (ATSDR 1993 ). Chronic exposure can result in fatigue, gastrointestinal distress, anemia, neuropathy, and skin lesions that can de velop into skin cancer in mammals. It can cause death in soil microb iota and earthworms. Cancer-causing and genetic mutation-causing effects occur in aquatic organisms, with those effects including behavioral impairments, growth reduction, appetite loss, and metabolic failure. Aquatic bottom feeders are more susce ptible to arsenic. In birds tolerance to arsenic varies among species, but effects include destruction of gut blood vessels, blood-cell damage, muscu lar incoordination, debility, slowness, jerkiness, falling, hyperactivity, fluffed feathers, drooped eyelids, immobility, seizures, and systemic, growth, behavioral, and reproducti ve problems (Stanley et al. 1994 ; Whitworth et al. 1991 ; Camardese et al. 1990)

. Inorganics

Aluminum Arsenic Barium Cadmium Chromium Copper

Cyanide Lead Manganese Mercury Nickel Selenium

Silver Thallium Zinc

Organics

Pesticides PAHs PCBs Dioxins 

## Region 5 Superfund htt p ://www.e p a. g ov/R5Su p er/ecolo gy /tox p rofiles.htm Last u p dated on Wednesda y, December 28

, 2011 

### Pa g e 1 of 8 Ecolo g ical ToxicityInformation | Re g ion 5 Superfund | US EPA

9/18/2012 http ://www.e p a. g ov/R5Su p er/ecolo gy/tox p rofiles.htmBarium

Elevated levels of barium can induce a wi de range of effects in mammals including gastrointestinal distress, muscu lar paralysis, and cardiovascul ar effects. Barium is does not bioaccumulate , and concentrations in higher species rarely exceed 10 mg/kg (Moore 1991 ).

Cadmium Cadmium is highly toxic to wildlife; it is cancer-causing and tera togenic and potentially mutation-causing, with seve re sublethal and lethal effects at low environmental concentrations (Eisler1985a ). It is associated with incr eased mortality, and it effects respiratory functions, enzyme levels, mu scle contractions, growth reduction, and reproduction. It bioaccumulatesat all trophic levels, accumulating in the livers and kidneys of fish (Sindayigaya, et al. 1994 ; Sadiq 1992 ). Crustaceans appear to be more sensitive to cadmium than fish and mollusks (Sadiq 1992 ). Cadmium can be toxic to plants at lower soil concentrations than ot her heavy metals and is more readily taken up than other metals (EPA 1981 ). On the other hand, some insects can accumulate high levels of cadmium without ad verse effects (Jamil and Hussain 1992 ).

Chromium There is no signific ant biomagnification of chromium in aquatic food webs (ATSDR, 1993 ). However, there are a wide range of ad verse effects in aqua tic organisms. In benthic invertebrates there has been observ ed reduced fecundity and survival, growth inhibition, and abnormal movement patt erns (U.S. EPA 1980b). Fish experienced reduced growth, chromosomal aberration s, reduced disease resistance, and morphological changes.

The toxic effects of chromium are primarily found at the lower trophic levels. The main potential ecological impacts result from directexposure of algae, benthic invertebrates, and embryos and fingerlings of freshwat er fish and amphibians to chromium. Chromium may bioaccumulate in algae, ot her aquatic vegetation, and invertebrates

, but it does not biomagnify. Ch romium inhibits growth in duckweed and algae, reduces fecundity and survival of be nthic invertebrates, and redu ces growth of freshwater fingerlings. It is cancer-causing, mutation-causing, and teratogenic. Chromium exists in two oxidation states in the environment: tr ivalent (+3) and hexavalent (+6), the latter of which is more toxic. Chro mium+6 is readily converted to chromium+3 in animals, which appears to protect higher organisms from the effects of low level exposures (Eisler 1986 ).

Copper Copper is a micronutrient and toxin. It stro ngly adsorbs to organic matter, carbonates and clay, which reduces its bioavailability . Copper is highly toxic in aquatic environments and has effect s in fish, invertebrates , and amphibians, with all three groups equally sensitive to chronic toxicity (U.S. EPA 1993 ; Horne and Dunson 1995 ). Copper is highly toxic to amphibians (including mortality and sodium loss), with adverse effects in tadpoles an d embryos (Horne and Dunson 1995 ; Owen 1981 ). Copper will bioconcentrate in many different organs in fish and mollusks (Owen 1981 ). There is low potential for bioconcentration in fish, but high potential in mollusks. Copper sulfate and other copper compounds ar e effective algaecides (free copper ions are the lethal agent). Single-cell and filamentous algae and cyanobacteria are particularly susceptible to the acute effects, which include reductions in photosynthesis and growth, loss of photosyn thetic pigments, disruption of potassium regulation, and mortality. Sensitive algae may be affected by free copper at low (parts per billion) ppb concentrations in freshwater.

There is a moderate potential for bioaccumulation in plants and no biomagnification.Toxic effects in birds in clude reduced growth rates, lowered egg p roduction

, and develo p mental abnormalities. While mammals are not as sensitive to 

### Pa g e 2 of 8 Ecolo g ical ToxicityInformation | Re g ion 5 Superfund | US EPA

9/18/2012 http ://www.e p a. g ov/R5Su p er/ecolo gy/tox p rofiles.htmcopper toxicity as aquatic organisms, toxicity in mammals includes a wide range of animals and effects such asliver cirrhosis, necrosis in kidneys and the brain, gastrointestinal distress, lesions, low blood pressure, and fetal mortality. (ATSDR 1990c ; Kabata

- Pendias and Pendias1992 ; Ware 1983 ; Vymazal 1995 ).

Cyanide Cyanide toxicity is caused by the free cyanid es (HCN and CN-) that inhibit cytochrome oxidase and thereby suppress aerobic resp iration. Fish are the most susceptible organisms - sensitive species exhibit chronic and lethal ef fects at as low as 5 to 7 grams/liter (chronic) and 20 to 76 grams/liter(lethal), respectively. The toxicity of complex cyanides is usually, but not always , low, but the degradation products often include free cyanides which are toxic. Fr ee cyanides readily degrade in the open environment but persist in groundwater. They do not bioaccumulate . Sublethal effects in fish include reduced reprod uctive capacity (decreased egg number and viability, and reduced embryo and larval survival), impair ed swimming ability, altered growth, and hepatic necrosis. Free cyanides are phytotox ic at higher concen trations than those associated with adverse effe cts in fish. Mammals are less sensitive than fish, and are relatively tolerant of intermitte nt sublethal exposures (Eisler1991 ).

Lead Lead is cancer-causing, and adversely effects reproduction , liver and thyroid function, and disease resistance (Eisler 1988b ). The main potential ecological impacts of wetland contaminants result from dire ct exposure of algae, benthi c invertebrates, and embryos and fingerlings of freshwater fish and amphibians to lead. It can be bioconcentrated from water, but does not bioaccumulate and tends to decrease with increasing trophic levels in freshwater habitats(Wong et al. 1978; Eisler 1988b ). Lead adversely affects algae, invertebrates, and fish. There are al so limited adverse effects in amphibians, including loss of sodium, reduced learning capability, and developmental problems (Horne and Dunson 1995 ; Freda 1991). Fish exposed to hi gh levels of lead exhibit a wide-range of effects incl uding muscular and neurol ogical degeneration and destruction, growth inhibition, mortality, reproductive problems, and paralysis (Eisler 1988b ; EPA 1976 ). Lead adversely affect s invertebrate reproduc tion; algal growth is affected. Lead partitions primarily to sedi ments, but becomes more bioavailable under low pH, hardness and organic matter co ntent (among other factors). Lead bioaccumulates in algae, macrophytes and benthic organisms, but the inorganic forms of lead do not biomagnify.

At elevated levels in plants, lead can ca use reduced growth, phot osynthesis, mitosis, and water absorption (Eisler 1988b ). Birds and mammals suffer effects from lead poisoning such as damage to the nervous system, kidneys, liver, sterility, growth inhibition, developmental retardation, an d detrimental effects in blood (Eisler 1988b ; Amdur et al. 1991 ). Lead poisoning in higher organisms has been associated with lead shot and organolead compounds, but not with food chain exposure to inorganic lead (other than lead shot, sinkers or paint) (Eisler 1988b ). There are complex interactions with other contaminants and diet. Lead poisoning in higher organisms primarily affects hematologic and neurol ogic processes.

Manganese Elevated levels of manganese in birds have been shown to cause the following effects: decreased hemoglobin, anemia, reduced growth; in mammals, effects include alterations of brain chemicals, gastric irritation, delayed testicular development, low birth weights, behavioral change s, and muscular weakness (ATSDR 1991 ).

Mercury Mercury is a mutagen (mutation-causing), teratogen, and carcinogen (cancer-causing), with toxicity and environmen tal effects varying with the form of mercury, dose, and route o f in g estion

, and with the ex p osed or g anism's s p ecies

, sex
, a g e
, and g eneral 

### Pa g e 3 of 8 Ecolo g ical ToxicityInformation | Re g ion 5 Superfund | US EPA

9/18/2012 http ://www.e p a. g ov/R5Su p er/ecolo gy/tox p rofiles.htmcondition (Eisler, 1987a , Fimreite 1979 ). There is a high pote ntial for bioaccumulation and biomagnification with mercury, with biomagnified concentrations reported in fish up to 100,000 times the ambient wa ter concentrations (Eisler 1987a , Callahan et al. 1979 ). Methylmercury is the most toxic form. Inorganic mercury is methylated primarily by bacteria in both anaerobic an d aerobic environments. The organic mercury compounds are more readily absorbed an d poorly excreted in comparison with inorganic forms. The primary targets of acute exposures are the central nervous system and kidneys in fi sh, birds and mammals.

In invertebrates, effects ra nge from non-observable to chromosomal abnormalities in some flies and reduce d segment regeneration in worms (Eisler 1987a ). Mercury can inhibit frog metamorphosis and has many effects in fish. In water, at concentrations at or well below even 1 ppb (part-per-billion), mercury can cause effects including: loss of appetite, brain lesions, ca taracts, abnormal motor coordination, and behavioral changes (MacDonald 1993 ). There are also effects on reproduction, growth, behavior, metabolism, blood chemistry, osmoregulation , and oxygen exchange at relatively low concentrations of mercury (Eisler 1987a ). Juveniles are commonly more susceptible than adults.

Upper trophic level fish, birds and mammals are particularly vulnerable because of the pronounced biomagnification of organomercury (Eisler 1987a ). There are numerous effects in birds, including delayed testicular developmen t, altered mating behavior, reduced fertility, reduced survivability and growth in young, and gonadal atresia. In mammals, it has been shown that mercury can cause ataxia, apha gia, tremors, and diminished movement c oordination (ATSDR 1994 ). There are varied neurological and reproductive effects as well (Cagiano etal. 1990 ; Khera et al. 1973 ).

Nickel Nickel is cancer-causing (car cinogen) and mutation-causing (mutagen). Some observed effects of nickel in aqua tic environments include tissu e damage, genotoxicity, and growth reduction (Environment Canada 1994a ). Mollusks and crustaceans are more sensitive than other organisms.

Selenium Selenium undergoes bioconcent ration, bioaccumulation, and biomagnification as trophic levels increase (Taylor et al., 1992 ). It can enter the food web through both sediments and surface water. Elevated levels cause growth reduction in green algae (Eisler 1985b ). In other aquatic organisms, the following adverse effects have been observed: loss of equilibrium and other neurological disorders, liver damage, reproductive failure, reduced growth, reduced movement rate , chromosomal aberrations, reduced hemoglobin and increased whit e blood cell count, and ne crosis of the ovaries.

Silver Silver may biomagnify in some aquatic invertebrates (Adriano 1986). However, it is highly toxic to aquatic organisms (EPA 1992 ). Elevated concentrations can cause larval mortality, developmental abnormalities, and reduced larval growth in fish (Klein

MacPhee et al. 1984 ); growth reduction in juvenile mussels (Calabrese et al. 1984 ); and adverse effects on reproduc tion in gastropods (Nelson et al. 1983 ). There are some indications of toxicity in plants. However, there are other reports suggesting that silver is not highly phytotoxic. Silver is toxic to soil microbes, thus inhibiting biotransformation (ATSDR 1990b ). Effects on mammals include pulmonary edema, congestion, and mortality.

Thallium Low rates of bioconcentration may occur in aquatic systems and thallium may be as toxic as copper on a weight basis (Zitko et al. 1975 ). Thallium can cause reductions in larval fish growth and percent embr yo hatchability and mortality (LeBlanc and Dean 1984 )

. 

### Pa g e 4 of 8 Ecolo g ical ToxicityInformation | Re g ion 5 Superfund | US EPA

9/18/2012 http ://www.e p a. g ov/R5Su p er/ecolo gy/tox p rofiles.htmZinc In many types of aquatic plan ts and animals, growth, surviv al, and reproduction can all be adversely affected by elev ated zinc levels (Eisler 1993 ). Zinc in aquatic systems tends to be partitioned into sediment and less frequently dissolved as hydrated zinc ions and organic and inorga nic complexes (MacDonald 1993 ). Zinc is toxic to plants at elevated levels, causing adverse effects on growth, survival, and reproduction (Eisler 1993 ). Terrestrial invertebrates show sensitivity to elevated zinc levels, with reduced survival, growth, and reproducti on. Elevated zinc levels can cause mortality, pancreatic degradation, reduced growth, and decrea sed weight gain in birds (Eisler 1993 ; NAS 1980); and elevated zinc can cause a wide range of problems in mammals including: cardiovascular, developmental, immunological, liver and kidney problems, neurological, hematological (blood problems), pancreatic, and reproductive (Eisler 1993 ; Domingo 1994 ).



## ORGANICS

POLYCHLORINATED BIPHENYLS (PCBs)

PCBs are mutation-causing, ca ncer-causing, and teratogenic. They are readily absorbed through the gut, respiratory system, and skin in mammals and will concentrate in the liver, blood, muscle, adipose (fatty) tissue, and skin (Eisler 1986). Mutation tends to decrease with increasing chlorination (U.S. EPA 1980).

In general, in aquatic systems, increased toxicity is associat ed with increasing exposure, younger developmental stages, crustaceans, and lower chlorinated biphenyls (Eisler 1986 ). An increase in somatic (non-reproductive cell) mutations have been observed in ostrich ferns (Matteuccia struthiopteris).

Toxic effects in avian species included the fo llowing: morbidity, tremors, upward pointing beaks, muscular incoordination, and he morrhagic areas in the liver (Eisler1986 ). Other sublethal effects include delaye d reproduction and chromosomal aberrations in Ringed Turtledoves; courtship and nestbuilding behavioral impairments in Mourning Doves; reduced hatchability in chicken eggs; and decline in sperm concentration in American Kestrels. However, birds tend to more resistant to ac ute exposure than othe r groups: no adverse reproductive effects were observed in Screec h Owls fed 3 ppm PCB diets or in Japanese Quail, Northern Bobwhite s, and Mallard Ducks.

Mink are very sensitive to PCBs, with concentrations as low as 0.1 mg/kg dietary fresh weight producing an LD-50 (lethal dose - 50: the level of contamination at which 50% of the sample population dies) in 3 months and complete reproductive in hibition among the survivors (Eisler 1986 ). Other effects include anorexia, weight loss, and lethargy. On the other hand, compared to mink, the Europe an ferret is highly resistant to PCBs. Rhesus monkeys are extremely sensitive to PCBs, with an increase in stillborns and abortions, lowered birth rates, hyperpigmentation, skin eruptions, eye pr oblems, and altered behavioral patterns.

There are a number of effects ob served in aquatic or ganisms due to exposure to PCBs (Eisler
1986 ). Those effects include growth reduction in algae and brook trout; reduced egg survival and reduced fertilization success in flounder, minnow s, sea urchins (prior to fertilization, eggs were more resistant to PCBs at insemination and afterwards); and complete reproductive failure in brook trout. Cancer-causing effects and biochemical perturbations were observed in trout liver cells and marine fi shes; with anemia, hyperglyce mia, and altered cholesterol metabolism in brown trout fed di ets with 10 PPM PCBs (U.S. EPA 1980). 

### Pa g e 5 of 8 Ecolo g ical ToxicityInformation | Re g ion 5 Superfund | US EPA

9/18/2012 http ://www.e p a. g ov/R5Su p er/ecolo gy/tox p rofiles.htmPESTICIDES

DDE is bioavailable to soil invertebrates and plants and has been shown to bioaccumulate in some grains (Verma and Pillai 1991). It is also very persistent in aq uatic systems, absorbing strongly to sediments, and bioconcentrating in aquatic organisms, including fish and other organisms (HSDB 1997 ). DDE tends to bioconcentrate in lower-trophic levels and will accumulate in food webs. DDT is toxic to ma ny types of aquatic or ganisms, even at low concentrations.

Heptachlor and gamma-BHC are both highly toxic to aquatic invertebrates (EPA 1980 ). However, although fish are less susceptible to heptachlor than invertebrates, gamma-BHC is highly toxic to fishes as well. Birds show a wide range of susceptibility to pesticides: dieldrin (less toxic than in aquatic or ganisms); heptachlor (moderately to highly toxic); gamma-BHC (slightly to moderately toxic); DDT (slightly to non-toxic). However, DDT causes eggshell thinning and embryo mortality, especially in pr edatory birds. There is also courtship behavior changes and other reproductive impairments (EXOTOXNET 1996).

DDT and its metabolite DDE are highly persistent and lipophilic compounds subject to pronounced biomagnification. The extremely low water solubilities result in strong adsorption to soil particles and very low leaching losses. Th e main physical causes of attenuation of soil DDT are volatilization (estimated half-life of 100 days) and eros ion. Microbes biodegrade DDT to DDE and DDD under aerobic (with oxygen) and anaerobic (without oxygen) conditions, respectively. Both metabolites are more pers istent than DDT. Plants absorb DDT and its metabolites from soil, but they are poorly transl ocated and remain primarily in the roots. The eating of leaves is therefore no t a significant route of exposure to soil DDT. Th e toxicity of DDT to earthworms is low (Edwards and Bohlen 1992 ), so bioaccumulation by earthworms is a significant route of exposure to vermivoresand can result in lethal doses (Barker 1958 ).

DDT and DDE are moderately toxic to rodents wi th oral LD50s in the low to high 100s mg/kg bw. However, DDT is a cumulative poison, and the chronic lethal dose may be substantially less than the acute lethal dose, for example, the chronic minimum lethal dose in mallards is 50 mg/kg bw/day, only 2% of the acute LD50 (Tucker and Crabtree 1970). DDT is a neurotoxin that affects the cent ral nervous system by increasi ng neurotransmitter release, disrupting neural ion regulation, and inhibiting neural ATPase activities. Symptoms include excitability, tremors, convulsion s and death. Chronic effects ar e of greater significance for higher organisms than acute effects. DD T adversely affects avian and mammalian reproduction by eggshell thinning, infertility, and embryo- and fetoto xicity. The effects may be related to the estrogenic activity of o,p' -DDT and o,p'-DDE. DDT and DDE are also cancercausing in rodents (ATSDR 1994b ).

DIOXINS

The most toxic of the chlorinated dio xin isomers is 2,3, 7,8-TCDD (Eisler 1986c ). It has been associated with lethal, cancer-causing, terato genic, reproductive, mutation-causing, tissue damaging, and immunotoxic effect s. In fish, the fo llowing effects were observed: reduced growth, fin necrosis, death, declining interest in feeding (5-8 days postexposure), skin discoloration, reduce d resistance to fungal infestations, reduced swimming, teratogenesis, tissue damage, degeneration and necrosis of the liver in fry, and opercular defects in fry. In general, older and larger fish die last; and smaller or younger specimens succumb first. Bioaccumulation does occur in fish. Among fish, bo dy burdens of 2,3, 7,8-TCDD increased with increasing concentration in the water column and with incr easing duration of exposure; 

### Pa g e 6 of 8 Ecolo g ical ToxicityInformation | Re g ion 5 Superfund | US EPA

9/18/2012 http ://www.e p a. g ov/R5Su p er/ecolo gy/tox p rofiles.htmon removal to uncontaminated water, less than 50% was lost in 109 days.

Invertebrates, plants, and amphibians were comparatively resistan t to 2,3,7,8-TCDD.

Birds exhibited the fo llowing effects from dioxins (Eisler 1986c): death, enlarged livers, severe emaciation, high accumula tions of uric acid salts in connective tissues, and fluid accumulations in the pericardial and abdominal cavities, excessive drinking, loss of appetite, hypoactivity, emaciation, weakness, debility, mu scular incoordination, increased reaction to stimuli, fluffed feathers, huddl ed position, unkempt appearance, falling, tremors, spasms, convulsions, necrosis, fatty degeneration, and immobility. Birds may bioaccumulate from fish prey, but dioxins do not appear to biomagnify.

In mammals, poisoning by 2,3,7, 8-TCDD is typically characterize d by loss of body weight and delayed lethality; large interspecies differen ces exist in lethal do sages and toxic effects (Eisler 1986c). For example, 2,3,7,8-TCDD produces pr ominent chloracne-type skin lesions in humans and monkeys, and severe liver damage in rats, mice, and ra bbits. Other effects include tissue damage, atrophy of the thymus , edema, hemorrhagic tracheitis, pleural hemorrhage, and dystrophic lesions of the liver, skin hyperkeratosis, gastric ulcers, and lung and kidney lesions, teratogenesis, carcinogenesis (in th e liver, pharnyx, lungs, skin, and thyroid), and fetotoxicity. Suppression of thymus -dependent cellular immunity, particularly in young animals, may contribute to their death. Developing mammalian fetuses are especially sensitive to 2,3,7,8-TCDD, an d maternal exposure results in increased frequencies of stillbirths. Among live births, exposure to 2,3,7, 8-TCDD produces teratogenic effects such as cystic kidney, cleft palate, and spinal column deformities; dioxin poisoning also produces decreased litter size at birth, increased numberof stillborns, and redu ced survival and growth of young in both the Fl and F2 generations (f irst and second generations of offspring--e.g., children and grandchildren of an imals exposed to a chemical). Higher dose level in monkeys for extended periods (i.e., 500 ppt in diets equ ivalent to about 0.011 ug /kg body weight daily for 9 months) caused death (63%) or, among sur vivors, abortion, chlora cne, nail loss, scaly and dry skin, and progressive weakness. Most treated monkeys remained fairly alert to external stimuli until just prio r to death. On removal from the 500 ppt 2,3,7, 8-TCDD diet and transfer to an uncontaminated diet, a severely affected monk ey became pregnant and gave birth to a well-developed infant after an uneventful gestation. This suggests that some 2,3,7,8-TCDD damaging effects are not permanent.

POLYCYCLIC AROMATIC HYDROCARBONS (PAHs)

PAHs are highly potent carcinogens that can produce tumors in some organisms at even single doses; but othe r non-cancer-causing effects are not well understood (Eisler 1987b ). Their effects are wide-ranging within an organism and have been found in many types of organisms, including non-human mammals, birds, invertebrates, plants, amphibians, fish, and humans. However, their effe cts are varied and so genera lizations cannot be readily made. It has been shown that the fungus Cunn inghamella elegans can inhibit the mutationcausing properties of various PAHs, includin g: benzo(a)pyrene an d benzo(a)anthracene. Effects on benthic invertebrate s include inhibited reproduction , delayed emergence, sediment avoidance, and mortality. Fish exposed to PAH contamination have exhibited fin erosion, liver abnormalities, cataracts, and immune system impairments lead ing to increased susceptibility to disease (Fabacher et al. 1991 ; Weeks and Warinner 1984 ; 1986 ; O'Conner and Huggett 1988 ).

Mammals can absorb PAHs by in halation, dermal contact, or (more poorly) ingestion (Eisler 1987b ). Plants can absorb PAHs from soils thro ugh their roots, and translocated them to 

### Pa g e 7 of 8 Ecolo g ical ToxicityInformation | Re g ion 5 Superfund | US EPA

9/18/2012 http ://www.e p a. g ov/R5Su p er/ecolo gy/tox p rofiles.htmother plant parts such as developing shoots. Uptake rates are generally governed by PAH concentration, PAH water solubility, soil type, and PAH physicochemical state (vapor or particulate). Lower molecular weight PAHs are absorbed more readily than higher molecular weight PAHs. PAH-induced phytotoxic effects are rare, howerver the database on this is limited. Some higher plants can catabolize PAHs, but this metabolic pathway is not well defined. Certain plants contain substances that can protect against PAH effects, inactivating their cancer-causing and mutation -causing potential. Additionally, PAHs synthesized by plants may act as growth hormones.

In aquatic systems, PAHs tend towards increa sed toxicity with incr eased molecular weight (Eisler 1987b ). In addition, although the rate of uptake from the environment is variable among species, bioaccumulati on tends to be rapid.

Adsorption of PAHs in soil is directly proportion al to soil organic matter (OM) content and the Kow of the PAH (greater in high molecular weig ht (HMW) PAHs than in low molecular weight (LMW) PAHs, and is inversely proportional to so il particle size (roughly 2 orders of magnitude greater on silts and clays as compared with sands). LMW PAHs have higher volatilization rates and are more readily leached as compar ed with HMW PAHs. Both LMW and HMW PAHs are microbially degraded, but the rates are higherfor the former probably because of weaker adsorption and greater bioavailability. Exampl es of soil half-lives are approximately 100-200 and 300-500 days for LMW and HMW PAHs, respect ively; however, they will be longer in hazardous waste sites toxic to bacteria. Plants absorb PAHs from so il, especially LMW PAHs, and readily translocate them to above-ground tissues. The concentrat ions in plants are substantially lower than in soil, and they ar e poorly correlated because of deposition and absorption of atmospheric PAHs. Eating of leaves (foliar herbivory) does not appear to be a significant route of exposure to soil PAHs. Bioaccumulation has been shown in terrestrial invertebrates and voles, earthworm levels were 30-60 times greater than soil concentrations (Gile et al. 1982), but PAH metabolism is suff icient to prevent biom agnification. The oral toxicity of PAHs ranges from very to modera tely toxic (50 to 1000s mg/kg bw) in rats. Many PAHs are cancer-causing, producing tumors in epithelial tissues in "practically all animal species tested" (Eisler 1987b ). Other effects in te rrestrial organisms ar e not well known, but may include adverse effects on reproduc tion, development, and immunity (ATSDR 1993c).

References 

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9/18/2012 http ://www.e p a. g ov/R5Su p er/ecolo gy/tox p rofiles.htm