Coastal Pollution: Effects on Living Resources and Humans - Chapter 5 pot

To make some sense of this, we can create some artificial categories and give a few examples, recognizing that interest in algal blooms is usually stimulated by the danger of toxic effec

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in Coastal Waters

INTRODUCTION: ALGAL BLOOMS AND

ALGAL TOXICITY

Algal blooms and algal toxicity are natural phenomena Why, then, should they have

a dominant position in a book concerned with coastal pollution? Two good reasons are: (1) augmentation of levels of nitrogen and phosphorous in coastal/estuarine waters — the basis for explosive population growth of planktonic algae — has been shown in many instances to be of human origin, and (2) human transport of toxic algal species to new habitats — with ships’ ballast water and by other commercial practices — has been demonstrated and is undoubtedly of common occurrence The frequency of occurrence, areal extent, and intensity of algal blooms seems

to be increasing on a global scale — a trend that would be expected as a consequence

of human contributions of nutrient chemicals to coastal/estuarine waters and of human participation in disseminating alien species Additionally, the list of types of algal toxins is gradually expanding, as is the geographic extent of reported toxic events and knowledge about the nature of the toxins produced

Population explosions of planktonic unicellular algae — so-called “algal blooms” or “red tides” (even though many of them are not red) have been observed for centuries and have in some instances caused shellfish in areas such as Puget Sound and northern New England to become temporarily toxic to humans Paralytic shellfish poisoning (PSP) is the best-known consequence of eating toxic bivalve molluscs, although several other types of poisoning have been described, and new ones are being identified Not all blooms are toxic, but many that are not may still

be harmful in a variety of ways — for example by reducing light penetration, by reducing dissolved oxygen levels, by forming mucilaginous aggregates, or by inter-fering with respiration of fish The overall perception is that many, if not most, algal blooms can be harmful, but not all harmful blooms are toxic

To make some sense of this, we can create some artificial categories and give a few examples, recognizing that interest in algal blooms is usually stimulated by the danger of toxic effects on humans, usually from eating contaminated shellfish However, as was pointed out in a recent excellent review (Shumway 1990), fish and shellfish (and other animals) may be affected severely by some of the algal toxins

I have identified, for descriptive purposes, several not–mutually exclusive categories that seem to encompass most but probably not all of the kinds of algal blooms that have been reported Examples, in the form of vignettes from my long-term field 9677_book.fm Page 57 Monday, November 14, 2005 9:17 AM

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58 Coastal Pollution: Effects on Living Resources and Humans

notes, have been inserted occasionally in the following material, to bring some reality

to the artificial subdivisions

ALGAL TOXINS

Some algal species may produce biotoxins that affect humans as well as marine animals Such toxin-producing organisms, when present in abundance, may be consumed by shellfish, plankton, and plankton-eating fish — sometimes causing fish mortalities and often rendering fish flesh toxic to humans and marine mammals Five principal types of toxins have been described, based on their effects on humans One (ciguatera) is found in tropical and subtropical fish flesh and is very toxic to humans; another, neurotoxic fish poisoning (NTP), is found in fish and shellfish; and three are found principally in shellfish: paralytic shellfish poisoning, diarrhetic shellfish poisoning (DSP), and amnesic shellfish poisoning (ASP)

C IGUATERA F ISH P OISONING

The causative organism of ciguatera fish poisoning (CFP; CTX) is Gambierdiscus toxicus, an epibenthic high-light-intolerant species of dinoflagellate associated with macroalgae (Yasumoto et al 1977) It is common in shallow tropical and subtropical seas between latitudes 28ºN and 28ºS Ciguatera is often considered to be the most common form of toxin-based seafood illness in the world (Fleming et al 1998, 2000) Outstanding manifestations of ciguatera poisoning are neurological, with symptoms persisting for weeks, months, or years, resulting in disabilities and some-times fatalities

The incidence of ciguatera poisoning appears to be rising in Florida, the Carib-bean, and the Pacific The Gambierdiscus biotoxins pass up the food chain from herbivorous reef fish to larger carnivorous, commercially valuable species Ciguatera poisoning was traditionally limited to tropical regions, but modern improvements in refrigeration and transport have augmented commercialization of tropical reef fish and increased the frequency of this type of fish poisoning among consumers in temperate regions

Biomagnification of ciguatoxin at various trophic levels results in high concen-trations in species such as barracuda, groupers, and snappers, associated with coral reefs Damage to living corals, caused by pollution, dredging, temperature increase,

or other human activity, can encourage growth of the macroalgae that Gambierdiscus

and other toxic microalgaeuse as substrates — leading eventually to an increase in fish toxicity (Gambierdiscus does not form pelagic blooms of motile individuals)

N EUROTOXIC F ISH P OISONING

Widespread, often seasonal toxic algal blooms can cause extensive fish mortalities, which may occur annually or at least sporadically Probably the best documented are seasonal outbreaks of neurotoxic poisoning (NTP) of fish and shellfish in the eastern Gulf of Mexico and particularly on the west coast of Florida — beginning early in the 20th century and caused by blooms of the dinoflagellate Gymnodinium

9677_book.fm Page 58 Monday, November 14, 2005 9:17 AM

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Harmful Algal Blooms in Coastal Waters 59

breve (now called Karenia brevis; Daugbjerg et al 2000).* Aided by the Gulf Stream, this neurotoxin-producing organism, traditionally a problem only in Florida, caused closures of major shellfish harvesting areas in North Carolina and South Carolina

in 1987 and 1988 Hundreds of Atlantic dolphin died in 1988, probably due to the neurotoxin present in fish consumed by the mammals

So the neurotoxins may be consumed by shellfish, plankton, and plankton-eating fish, causing mortalities and rendering their flesh toxic to humans and marine mammals — and their toxins may also be aerosolized by wave action and onshore winds, to affect humans by still another route — as experienced recently in Florida

Algal Toxins Make Unwelcome Landfall in Florida

A late afternoon cocktail party on Thanksgiving weekend 2002 at a beach-front house in Sebastian, Florida, came to an abrupt and unpleasant end when onshore winds carrying sea spray increased in intensity One participant described the episode vividly as follows:

“It was thoroughly disagreeable Everybody was coughing and sneez-ing I had an almost instantaneous burning throat, and then began gagging with every breath We all left the party quickly, but the aftereffects in my case involved more than malaise — I was unable to get out of bed the next day.”

Up and down that section of Florida’s east coast, many people — especially beachgoers and surfers — suffered from a variety of ocean-related ills — especially irritation of eyes and throat, coughing, and sneezing The problem persisted for the rest of November and into December 2002, apparently caused

by a bloom of Karenia brevis (aka Gymnodinium breve), a well-known neuro-toxic alga most common on the opposite (west) coast of Florida Reports of oxygen depletion and fish kills were part of the story, with small inshore fish species most commonly involved A beachfront employee (describing the local situation at Cocoa Beach) stated, “the water feels slimy, and sometimes there are dead fish in it.”

From Field Notes of a Pollution Watcher

(C.J Sindermann, 2003)

A problem that is possibly equal in intensity to effects of algal neurotoxins in southeastern U.S waters is that of PSP in northeastern and northwestern Canada and United States, caused by blooms of dinoflagellates of the genus Alexandrium

* The taxonomy of the microalgae has been in what can be labeled euphemistically as a dynamic state, especially during the past 2 decades Some proposed changes in specific and generic designations have been accepted quickly, and others more slowly, resulting in a high degree of confusion on the part of the nonspecialist.

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Intensive toxin monitoring has resulted in frequent closure of shellfisheries on these North American coasts for more than half a century The toxin may also cause fish mortalities Sea herring (Clupea harengus) were killed in large numbers in the Bay

of Fundy in the late 1970s by feeding on zooplankton (cladocerans and pteropods) that had fed on the toxic algae In a later experimental study, red sea bream (Pagrus major)larvae and juveniles were affected, and many died after feeding on plankton containing the toxins

Poisoning by Alexandrium toxins was also suspected to be a cause of humpback whale mass mortalities (12 to 14 individuals) on Georges Bank off Massachusetts

in 1987 and again in 2003 (Geraci et al 1989, Pearson 2003) The speculation was made that the whales had been feeding on mackerel in which the toxin had been accumulated (Paralytic shellfish poisoning and other shellfish-borne biotoxins will

be explored further, but from a molluscan perspective, in the following section.)

S HELLFISH- B ORNE B IOTOXINS

Shellfish have been identified as passive carriers in a number of outbreaks of human illnesses due to toxins of algal origin The list begins with the well-known and widespread paralytic shellfish poisoning (PSP), which is a consequence of blooms,

in temperate coastal waters, of toxic dinoflagellates of the genus Alexandrium (for-merly Gonyaulax), and with neurotoxic shellfish poisoning (NSP), caused by blooms

of Karenia brevis (formerly Ptychodiscus brevis and, before that, Gymnodinium breve), responsible also for massive fish kills in the Gulf of Mexico Next in order

of appearance is diarrhetic shellfish poisoning (DSP), caused by other genera of toxic dinoflagellates (Dinophysis, Prorocentrum, and others) This form of poisoning was first reported in Europe in 1961 (Korringa & Roskam 1961) It became important

in the late 1970s, after outbreaks in Japan and Europe, and persisted as a significant problem in the 1980s (Kat 1987) In December 1987, a “new” toxin, domoic acid, which causes amnesic shellfish poisoning (ASP), was found in mussels from Prince Edward Island in the Gulf of St Lawrence and was responsible for 129 cases of poisoning and 2 deaths in Canada (Pirquet 1988) Domoic acid can affect the brain and the nervous system of humans It is concentrated, during blooms, in the digestive gland of shellfish, especially mussels, and (during the Canadian outbreak) its origin was reported to be a persistent bloom of the diatom Pseudo-nitzschia multiseries in mussel culture areas of Prince Edward Island Table 5.1 summarizes key information about these common types of shellfish poisoning, as well as ciguatera fish poisoning The history of changes in the status of the various fish and shellfish poisonings includes the following:

PSP — Recurrent PSP outbreaks now affect the states of Maine, New Hamp-shire, Massachusetts, Oregon, Washington, and Alaska PSP problems constrain the development of a shellfish industry in Alaska Offshore shellfish on Georges Bank off New England became toxic for the first time in 1989 and have remained toxic since then Low levels of PSP have been found in Rhode Island, Connecticut, and New York In 1987, 19 whales are thought to have died from PSP toxin contained

in mackerel they had consumed — a significant event, since PSP was previously believed to be a problem principally in shellfish Resting cysts of PSP-toxin–pro-9677_book.fm Page 60 Monday, November 14, 2005 9:17 AM

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Harmful Algal Blooms in Coastal W

TABLE 5.1

Common Types of Poisoning by Biotoxins Acquired by Consuming Fish and Shellfish

Illness Symptoms Cause Description Useful References

Paralytic shellfish poisoning

(PSP)

Numbness of lips, face, and extremities; visual disturbance;

staggering gait; difficulty breathing; paralysis

Species of the dinoflagellate

About 12 forms purine-derived saxitoxins; water soluble; acts by blocking sodium channel needed

to transmit nerve impulses

Bricelj & Shumway 1998

Neurotoxic shellfish

poisoning (NSP)

Nonfatal but unpleasant neurotoxic symptoms; strong action on cardiovascular system

Toxins have unusual polycyclic ether skeletons

Schneider & Rodrick 1995;

Fletcher, Hay, & Scott 1998, 2002

Diarrhetic shellfish

poisoning (DSP)

Cramps; severe diarrhea; nausea;

vomiting; chills; death rare

large, fat-soluble polyethers; can move across cell membranes and make them “leak”

Bricelj et al 1998; Gayoso, Dover, & Morton 2002

Amnesic shellfish poisoning

(domoic acid; ASP)

Nausea; vomiting; muscle weakness; disorientation; loss of short-term memory

Species of the diatom genus

Nonessential amino acid; mimics glutamic acid; affects brain and nervous system; found in digestive glands of contaminated shellfish

Wohlgeschaffen et al 1992;

Whyte, Ginther, & Townsend 1995

Ciguatera fish poisoning

(CFP)

Paralysis; respiratory failure;

death

(other species possibly linked to

carterae; Coolia monotis;

Ostreopsis spp., Prorocentrum spp.,

Neurotoxic microalga associated with tropical/subtropical macroalgae

Yasumoto et al 1980, Gillespie et

al 1985, Villareal & Morton 2002

from Chilean mussels (Lewis 2000).

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ducing species from bottom sediments in New England waters were found to be 10 times more toxic than were motile stages Cysts may be ingested by shellfish, causing toxicity even when blooms are not apparent

DSP — Diarrhetic shellfish poisoning, with diarrhea as the dominant symptom, was first described in Europe in 1961 and subsequently reported elsewhere in Europe and in Japan It must be noted, though, that shellfish-associated enteric disorders have a long history, and this type of poisoning may have been present much earlier but not diagnosed correctly In 1990, the first confirmed outbreak of DSP in North America occurred in Canada Two more outbreaks occurred in 1992 Scattered, unconfirmed cases of DSP have been positively reported in the United States, and the causative organisms have been positively identified in U.S waters

ASP — The toxin of amnesic shellfish poisoning (domoic acid) was detected

in Nantucket scallops in 1990 and 1991 Toxic Pseudo-nitzschia species have been identified in the Gulf of Mexico, and seabird mortalities in the state of California

in 1991 were linked to levels of the toxin found in the flesh of fish that had been consumed Also in 1991, the ASP toxin occurred in the state of Washington, where contaminated clams and crabs caused human illnesses The causative organisms have also been identified in U.S Atlantic coastal waters

PFIESTERIA — A TOXIC ALGAL PREDATOR

Some algal species may be toxic under certain environmental conditions, but not continuously so A dinoflagellate, Pfiesteria piscicida, and its relatives are examples

of such organisms Examined with great interest since the early 1990s, Pfiesteria, with effects in U.S east coast waters, has been found at times to be toxic to, and even predatory on, estuarine fish (Burkholder et al 1992, Noga et al 1993) Further-more, the organism has been reported to be toxic to humans as a consequence of environmental exposure, causing skin and neural disorders (Burkholder et al 1995)

The “Microbe from Hell”

It is a hot humid August morning in 1997 in the tiny fishing village of Shelltown, on the banks of the Pocomoke River — an insignificant waterway that forms the extreme southern boundary of Maryland’s Eastern Shore But some of the people on the street are not fishermen or even locals They look disturbingly like alien invaders, with metallic-appearing full-body protective clothing and with respirators dangling around their necks They are actually field technicians from the Department of Natural Resources, and they are here

to investigate a strange and frightening series of events in this little tributary

of Chesapeake Bay Fish — especially menhaden — are dying in large numbers, and many of the surviving individuals have conspicuous ulcerations on their skins But beyond this, and of much greater concern, people who had contacted the water near the fish kills have been reporting illnesses — disorientation, loss

of recent memory, nausea, and skin lesions.

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The fish kills are not that unusual; they have been occurring sporadically for most of the century in varying intensities and locations up and down the Atlantic coast from Long Island to Florida — to the extent that most coastal states have established fish kill reporting offices But fish kills that involve simultaneous outbreaks of human disease have not been reported before, and this is a matter of great interest to public health officials and politicians (and,

of course, to residents).

The culprit seems to be a single-celled aquatic organism discovered in 1988 and subsequently named Pfiesteria piscicida, a member of a mostly planktonic algal group known as dinoflagellates This is no ordinary member of the group.

It is an aggressive fish predator, and it is reported to secrete a toxin (or toxins) that immobilizes the fish, destroys portions of its skin, and kills it by disrupting its nervous system Individual fish that escape the lethal effects of the toxin often display evidence of the encounter in the form of skin lesions that develop into deep penetrating ulcers.

Fish kills of this type have been common further south in Pamlico Sound, North Carolina, since the early 1980s, and the presumptive cause — Pfiesteria

— has been studied there since the early 1990s Over half of all the fish kills

in those waters from 1991 to 1993 have been attributed to the toxic organism, and it has been identified in water and sediment samples from other Atlantic coastal states from Delaware to Alabama — as have high prevalences of skin ulcers in affected fish species.

Events in the Pocomoke River, a scenic two-hour drive from Washington, D.C., became a media focus in late summer of 1997 Scientists were interested because the reality of a dinoflagellate as an aggressive fish predator rather than

a passive, occasionally toxic algal form, represented a paradigm shift in their thinking; public health administrators had to be involved because of claims of human illnesses associated with the fish deaths; watermen and seafood dealers had to face substantial consumer resistance and lost income because of unsub-stantiated fears of toxin contamination of fish products; and politicians had to weigh their public positions and statements very carefully, because one of the underlying causes of the outbreak was thought to be excessive nutrient contam-ination from agriculture and from overloaded sewage treatment plants What a bonanza for an alert news reporter! Portions of the Pocomoke River and two other suspect rivers were closed by the governor of Maryland; public meetings were held at least weekly on the Eastern Shore during that period of uncertainty; and the U.S Congress rushed to prepare bills authorizing relatively huge sums (well in excess of 10 million dollars) for research and environmental monitoring Most of the funding will go, of course, to the Centers for Disease Control in Atlanta, because of the human health threat (fish and environment are always

“also-rans” in the quest for funds if human diseases are involved).

But then the onset of cool weather in the late autumn of 1997 seemed to reduce the activity of the “microbe from hell” (a newspaper headline writer’s invented appellation) and the event was banished to the back pages of the

“Washington Post” and the “Baltimore Sun” — with only occasional reawak-ening of interest when the various committees, commissions and investigative

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groups formed at the peak of the excitement made their reports Most of them pointed to excessive nutrient loading of rivers and sub-estuaries of Chesapeake Bay as a likely reason for the outbreak of Pfiesteria, although evidence was far from robust All the reports encouraged more research, especially on the human disease implications, the nature of the toxins produced, and the environmental factors responsible for the proliferation of the toxic form of the organism (and possibly its close relatives).

What we may be seeing in this small tributary of the Chesapeake Bay is a tiny segment of an expanding global problem — an increase in the frequency, intensity, and nature of harmful algal blooms.

From Field Notes of a Pollution Watcher

(C.J Sindermann, 1998)

Federal funding from several agencies resulted from the intense media attention

to the Pfiesteria outbreak in 1997 The possibility of human disabilities resulting from environmental exposure to toxins stimulated sizeable research grants from the National Institutes of Health and the Centers for Disease Control However, as might be expected, blooms of Pfiesteria did not recur to any significant extent in the years 1998 to 2003, although the causative organism (and some close relatives) have been identified in estuarine waters of the middle Atlantic states as far south

as the Florida border Toxic episodes with associated fish ulcerations and mortalities have not been reported

The availability of research funding has led to significant new information about

Pfiesteria piscicida The organism has been detected frequently in mid-Atlantic waters, but not in toxic form A second but nontoxic species, P shumwayae, has been recognized (Vogelbein et al 2002) Nontoxic forms of the second species, P shumwayae, were reported to attack and wound fish such as young menhaden, providing possible entry points for fungal spores, with subsequent development of ulcers In other reports, the ulcers thought to be caused by exposure to the toxins

of P piscicida were considered to be caused (at least in part) by invasion of the fungus Aphanomyces invadans

ALGAL BLOOMS AND AQUACULTURE

Algal blooms, toxic and nontoxic, in the vicinity of aquaculture production opera-tions may cause fish mortalities Farmed fish, especially Atlantic salmon, have been killed, often in large numbers, by such blooms Mortalities of farmed salmon in Scotland in 1979 and 1982 were caused by blooms of species of Olisthodiscus or

Chattonella These algae had been identified earlier in connection with unusual blooms, but occurrences were rare and geographically restricted Blooms of the naked dinoflagellate Gyrodinium aureolum were observed to cause mortalities of marine organisms in England in 1978, in Scottish salmon cages in 1980, and in wild

as well as captive fish on the coast of Norway in 1981 and 1982 A large bloom of 9677_book.fm Page 64 Monday, November 14, 2005 9:17 AM

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Chrysochromulina polylepsis caused extensive mortalities in sea cages (Bruno, Dear,

& Seaton 1989) Widespread blooms of this toxin-producing species occurred in the

waters adjacent to a number of North European countries during much of the 1980s,

seriously affecting salmon aquaculture (Vagn-Hansen 1989)

Some species of diatoms and spiny armored dinoflagellates may bloom in the

vicinity of sea cages, where they can cause fish mortalities from excess mucus

production and resulting suffocation Mortalities of farmed salmon in the U.S Pacific

Northwest due to blooms of the diatom Chaetoceros and the chloromonad

Het-erosigma have been a serious impediment to the development of this industry

Major destructive blooms have also occurred in many other parts of the world,

with severe effects on aquaculture Notable in this respect have been extensive and

recurrent blooms (especially in the 1970s and 1980s) in parts of the Seto Inland Sea

of Japan, which have affected yellowtail and sea bream production (Imai, Itakura,

& Ito 1991) Other sporadic outbreaks have had impacts on mussel culture in Spain

and Canada, and on bay scallop production in Long Island Sound (NY) waters

MUCILAGINOUS ALGAE

Some kinds of algal blooms may be accompanied by extensive mucous aggregations

that foul beaches and fishing nets and may cause bottom water anoxia, with

accom-panying mortalities of benthic animals Such mucilaginous blooms have occurred

in recent decades in the North Sea and the Adriatic Sea, caused respectively by the

diatoms Phaeocystis pouchetti and Skeletonema costatum Mucilaginous Phaeocystis

blooms in North Sea coastal waters have caused so-called “foam banks” on the

beaches of Germany, France, and the Netherlands Five acute Skeletonema episodes

have occurred in the northern Adriatic Sea (Croatian coast) since 1988 Each event

was characterized by areas of loose gelatinous mucous aggregates consisting largely

of extracellular polysaccharides Other diatoms (for example, Chaetocerus affinis)

and types of phytoplankton other than diatoms may produce polysaccharide exudates

under the proper environmental conditions (Heil, Maranda, & Shimizu 1993)

Some of the chemistry of mucilaginous blooms has been elucidated by research

done with Skeletonema in the Adriatic Sea (Thornton, Santillo, & Thake 1999)

These investigators theorize that drought conditions result in lower river flow and

limitation of nutrients and calcium in coastal waters Mucilage is produced by the

phytoplankton under those conditions and is stabilized to form a gel by contact and

intermixing with higher calcium levels offshore — leading to formation of extensive

aggregates, some of which move onto beaches or into shallow water, where fish and

bottom-dwelling animals may be killed

COASTAL/ESTUARINE AND OFFSHORE

ALGAL BLOOMS

Algal blooms of varying dimensions, persistence, and toxicity occur in

ever-increas-ing frequency in coastal/estuarine waters, where they may cause hypoxia or anoxia,

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with fish and shellfish mortality, or may cause decline in submerged attached

veg-etation as a consequence of decreased light penetration Here is a good example

“Brown Tide” in Long Island Waters

The New York Air National Guard plane made its final crisis response flight

for the month over the abnormally brown waters of Great South Bay on the

outer coast of Long Island It was late summer 1986 — the second year that

bays on the Island had been discolored and choked by the massive growth of a

planktonic microalgal species just recently identified as Aureococcus

anophag-efferens, an organism not previously known to cause blooms in that area of the

coast The findings from the day’s survey were grim: current abundance of the

toxic organism in the bay was 1,000,000,000 algal cells per liter, similar to

what it had been all summer, resulting in severe reduction of light penetration

of the water This had caused significant reduction in eel grass abundance and

distribution in Long Island bays, and profound disturbances in other

compo-nents of the shallow water ecosystem.

One of the animal species most affected by the algal bloom was the bay

scallop Argopecten irradians, the base for an important commercial shellfishery.

In the summer of 1985, when the bloom began, most of the scallop larvae had

died, resulting in a massive recruitment failure New York scallop landings in

that year were only 58% of the average for the preceding four years Natural

restocking was precluded by recurrence of the bloom in the summer of 1986,

and its reappearance in some previously affected areas in 1987 The concurrent

loss of critical eel grass habitat may serve to further inhibit reestablishment of

the Long Island bay scallop fishery.

The problem was not confined to Long Island waters The same alga,

Aureococcus anophagefferens, bloomed from Narragansett Bay, Rhode Island,

southward to Barnegat Bay, New Jersey, in 1985 It caused mortalities of mussels

Mytilus edulis in excess of 95% in Narragansett Bay, and significant growth

suppression in hard clams Mercenaria mercenaria in Long Island bays Mats

of dead eel grass littered the shores in New York and New Jersey.

The problem did not disappear with the passage of time, either A 1991

“NOAA News Bulletin” reported that an Aureococcus bloom had reoccurred in

eastern Long Island Sound in June of that year, with cell densities eight times

that known to harm marine animals Bay scallops larvae were again assumed

to have been killed by the early stages of the bloom

Major brown tides occurred along the south Texas coast from 1990 through

1992, and on the New Jersey coast in 1999 and 2000.

A relationship of recurrent algal blooms such as these to modifications by

humans of coastal/estuarine waters is often suggested, and some evidence exists.

Nutrient enrichment from agricultural runoff, sewerage outfalls, and some

industrial effluents may be involved, as may be the transport of toxic algae to

new locations in ships’ ballast water or with introduced marine animals

What-9677_book.fm Page 66 Monday, November 14, 2005 9:17 AM

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