lllution has the highest las been DAVID SAROKIN level of certainty mplias being caused U.S. Environmental Protection cated as Agency by pollution. a priOther populaWashington, DC 20460 mary or secondtions are also exary factor i n a JAY SCHULKIN periencing unnumber of largeUniversilyofpennsylvanio usual perturscale perturbab a t i o n s over a Philadelphia, PA 19104 tions to terrestrial broad geographic and aquatic poparea, but the role ulations, includ- In Part 1 the authors discuss of pollution in ing the bleaching aquatic populations; in Part 2 next these episodes is of c o r a l r e e f s : month they will discuss peturbatic more speculamass die-offs of in terrestrial populations. tive. dolphins and Species impacts seals; unusual phytoplankton S p e c i e s of blooms; cancer plants or animals epizootics (epiare subject to a demics) in fish; great number of population d e disruptive forces cline of amphibithat can dramatians, ducks, and cally alter, reother birds; and duce, and even impacts on fordecimate entire ests, especially populations red spruce a n d across a broad sugar maples. geographic scale. Chlorinated orSometimes t h e ganic pollutants sucll rclDD, y u I , G ~ U D U U Y C ~ U ~ W L S are obvious, as and acid rain are frequently cited as with the disappearance of the bufspecific pollutants of concern. Glo- falo from overhunting, or can be bal warming has also been hypothe- clearly identified, as was the case sized to be a pollution-related factor with the collapse of the Dutch Elm contributing to world-wide epi- tree population due to a virulent sodes of coral reef bleaching. fungus in the first half of this cenT h i s p a p e r reviews w h a t i s tury ( I ) . Other times, the reasons for known about the occurrence and a population's decline remain obcauses of these episodes, and evalu- scure. The most dramatic instance ates the degree to which available of this is the complete disappearinformation supports a conclusion ance of the giant reptiles at the end that a novel perturbation has actu- of the Cretaceous period. ally taken place, and pollution has In the past two decades, scientists caused or contributed to the distur- have observed a number of broadbance. An epizootic of fish tumors scale perturbations in ordinarily ~
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POPULATION DISTURBANCES Part I : Aquafic Popuh~fions 1476 Environ Scb Techno1 , VoI 26. No 8. 1992
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stable populations of plants and animals that have raised concerns about the impacts of pollution on the health of these populations. A few of these perturbations, such as the massive die-off of dolphins along t h e eastern shore of the United States in the summer of 1987, received considerable attention in the news media and resulted in widespread public alarm. Others, such as the dramatic decline of black sea urchins in the Caribbean, received little attention from the general public. These recent, large-scale perturbations are examined in this article. We have reviewed not only the scientific literature-which is often surprisingly meager-but also the journalistic and government reports that have provided much of the available information on these disturbances. All the events have several features in common: They cover hundreds or thousands of miles and can reasonably be considered regional or even global phenomena. They are without precedent in either the scientific literature or the collective “common knowledge” about such systems. There is no immediately obvious cause for the perturbation, although pollution is often suspected as a primary or contributing factor. Aquatic perturbations Large-scale perturbations in oceanic populations have received enough attention in recent years to have merited a categorical title: Major Marine Ecological Disturbances, or MMEDs (2). These, along with perturbations in certain fresh water populations, are described below. Dolphins On June 15, 1987, a bottlenose dolphin washed up onto a New Jersey beach, the first of about three expected strandings in the state during a typical season. Thirty days later. 47 dolphins had washed ashore on New Jersey beaches, and similar strandings were occurring along the entire east coast of the United States [Figure 1). In 11 months, at least 740 bottlenose dolphins were washed up on beaches from New Jersey to Florida, out of an inshore population estimated at 3000 to 5000. Because not all afflicted animals were necessarily washed ashore, the overall impact presumably w a s significantly higher: perhaps 50% of the popula-
enose dolphin strandings, U.S.East Coast, 1978-88 D
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tion died in the 1987-1988 episode (3). Other marine mammals also seemed to be affected the harbor porpoise and the humpback whale were stranded in numbers two and five times greater than in typical years although the overall number of animals involved was much smaller than for the bottlenose dolphins ( 4 ) . A dolphin die-off of this character and magnitude had never before been observed. Mass stranding of a single herd, localized in space and time, are not uncommon amongst cetaceans [though not often reported for dolphins). But a die-off characterized by hundreds of individual strandings over a thousandmile stretch of coast for a period of 11 months was unprecedented. In addition, the animals suffered from a range of symptoms that startled scientists familiar with diseases of marine mammals. Many had dermal lesions ranging from small, localized blisters to sloughed-off large areas of skin that exposed reddened areas of underlying dermis. The conditions were striking and had never before been observed. Scientists examining the dead animals reported that the “epidermis could be peeled back as easily as a covering of cellophane” 61, a condition that seemed clearly related to massive, systemic bacterial infection. Septicemia also undermined blood vessel integrity and resulted in widespread edema i n many organs. Internal lesions were widely noted in the lung, liver, pan-
1478 Envimn. Sei. Technol.. Vol. 28, No. 8, 1992
creas, and heart. Liver necrosis was common. Bacterial infection was widespread, even in freshly dead animals, and stemmed from numerous microorganisms ordinarily present in much smaller, benign concentrations. The symptoms suggested an opportunistic infection of already weakened animals. Viruses were also found in some animals, although the geographic and temporal patterns of mortality were considered uncharacteristic of viral infection. Animal tissues were assayed for a variety of toxins of both anthropogenic and natural sources. Tests for brevetoxin (a red-tide toxin) were positive in 8 out of 17 dolphins tested, as well as in a menhaden taken from the stomach of one dolphin and in fresh-caught menhaden. The results on fish other than menhaden were negative. Tests for synthetic organochlorine pollutants revealed three major categories of pollutants present in almost all animals tested DDTs, chlordanes, and FCBs. These contaminants were detectable in every blubber sample and in a very high proportion of liver tissue. The highest concentrations, all from the blubber of a single animal, were PCBs, 6800 ppm; DDE, 2000 ppm; and t-nonachlor, 400 ppm. and were amongst the highest values ever recorded in any animal tissue. Blubber concentrations in the tens and hundreds of parts per million were more typical in the other dolphins tested. Heavy
metals, in comparison, were routinely present, but not in concentrations deemed abnormally high. The research team examining the die-off concluded that brevetoxin poisoning was the most likely precipitating event leading to the dolphin deaths. Although Ptychodiscus brevis, the alga associated with brevetoxin formation, is ordinarily found in the Gulf of Mexico and not along the Atlantic coast, an unusual bloom of this organism did occur along the coast of North Carolina in October 1987 and is thought to be the source of the brevetoxin. The toxin accumulated in the tissue of fish, then was ingested by the dolphins, making them ill. The dolphins often appeared emaciated, indicating they were metabolizing their blubber reserves, which both reduced their buoyancy and insulation (adding to overall stress), and released stores of bioaccumulated pollutants, such as PCBs, which may have further exacerbated their condition. The combined impact led to immunoincompetence; they became vulnerable to opportunistic bacterial infection, which was the ultimate cause of death. A number of researchers have raised serious objections to this interpretation of the data (6-9). Bottlenose dolphins are common in the Gulf of Mexico, as are P. brevis red tides, yet no dolphin die-off of a similar magnitude or kind had ever been noted. Red tides are also often associated with massive fish kills, which were not present in any unusual numbers along the East Coast. Dolphins began dying in June in New Jersey, almost five months before and hundreds of miles from the North Carolina red tide bloom. The effects of brevetoxin on dolphins are unknown and are little described in other species, whereas PCB poisoning is known to impair functioning of the immune system and the liver and to cause skin lesions, all of which were observed in the diseased animals. A wide variety of additional pollutants, including brominated organics, have subsequently been identified in some of the tissue samples and may be contributing factors (R. Haebler, Narragansett Bay, RI, EPA Laboratory, personal communication). An alternative hypothesis is that a sudden influx of pollutants, perhaps from offshore dumping, was the poison that triggered a cascade of events in animals whose systems were already heavily laden with pollutants, leading to the die-off, In
this scenario, brevetoxin may or may not have been an important contributing factor. Since the 1987-88 die-off, two other episodes of dolphin mass mortality have received attention. In January and February 1990 at l e a s t 80 b o t t l e n o s e d o l p h i n s washed up along the Texas Gulf coast. In August of the same year, 50 striped dolphins washed up on the northeast shore of Spain’s Atlantic coast, and hundreds more washed ashore on Mediterranean beaches in Spain, France, and Italy in the next few months. The deaths have continued throughout 1991, and by some estimates the overall death toll is in the tens of thousands (1012).Viral infection appears to be the principal cause of the Mediterranean die-off (see discussion of seals, below). However, pollution is strongly suspected as a contributing factor. The rare vaquita or harbor porpoise of the Gulf of California is also considered imperiled by numerous threats, including pollution (13). Researchers are almost routinely finding high levels of contaminants in dolphin tissues during all die-off events. PCBs at concentrations of 500-3000 pprn were fairly common in the dead Mediterranean animals (14).These levels are considered extremely high; human tissue, in contrast, rarely contains more than 3 pprn of PCBs. DDT compounds averaged 432 pprn in the Mediterranean animals. Dolphins and other marine mammals may accumulate such high levels because they lack many of the enzymes necessary for metabolizing PCBs and related compounds; they may be particularly at risk because up to 80% of the body burden of PCBs of a mature female dolphin can be passed along to the first-born during lactation (15).
Seals At approximately the same time as the dolphin die-offs, seals were dying in great numbers in at least two locations. In autumn 1987, greatly weakened Lake Baikal (Siberia) seals were observed crawling ashore; by the following autumn, about 10% of the 80,000-100,000 population of Lake Baikal seals had died (16).No similar event had ever been observed in the lake in records extending back to the 1930s. In April 1988, large numbers of dead harbor seals (also known as common seals) and aborted seal pups were observed along the Danish coast of the Kattegat Strait. The
event spread throughout the North Sea, and seals died in great numbers in waters off the coasts of Denmark, Sweden, Norway, West Germany, Holland, and Great Britain. As many as 18,000 seals may have died to date, out of a total herd estimated at 44,000, with death rates of 60% in some areas. Gray seals have also died in large numbers, but not nearly with the same virulence (16). Unlike the dolphin die-offs, the primary cause of the seal deaths has been fairly well-established; both the North Sea and Lake Baikal seals died from a rampant viral disease, initially classified as canine distemper virus (CDV). The viruses causing the Lake Baikal outbreak appear indistinguishable from CDV, but the virus afflicting North Sea seals has been reclassified as a newly identified phocine distemper virus (PDV) (17). Why the virus, present in blood samples taken from seal populations in Greenland as early as 1984 (18), suddenly became virulent in 1987-88, and how similar outbreaks of virus struck in two such disparate locations, are questions that remain unanswered. Smaller populations are also faced with serious declines. Mediterranean monk seals have become extremely rare-perhaps 500 animals remain in the wild. A die-off of six animals in fall 1990 raised fears of an epizootic that could threaten the remaining population (13). There is some indication that factors other than viruses are involved in the seal epizootics. Veterinarians familiar with seal diseases have noted the extremely broad range of symptoms, infections, and systemic failure in the seals, possibly indicative of suppression of the immune system. Some researchers (16) have noted that intense and unusual phytoplankton blooms occurred in the North Sea at the same time as the onset of the harbor seal deaths (see discussion of blooms, below), and speculate that changes in nutrient loading and microbial activity may be related to the epizootic in as yet unspecified ways; other researchers reject this as unlikely to be significant over so large an area (19). Bioaccumulative pollutants may have played a triggering role, as well. As with the dolphin die-offs, contamination from PCBs and other industrial chemicals is common and is suspected as a contributing factor (20). Zakharov and Yablokov (21) found that the skulls of Baltic Grey seals born after 1960 had pronounced levels of asymmetry in al-
Environ. Sci. Technol., Vol. 26, No. 8, 1992 1479
most every character measured, when compared with the skulls of animals from a pre-1940 population, an effect they attributed to the heavy pollution of the Baltic beginning in the mid-1950s. Several researchers have noted historical correspondence between unusually warm waters and viral epizootics in seal populations, and have suggested that warm water increases the “hauling out” of seals onto rocks where they can more readily transmit infection. The possible role of global climate change in contributing to local warmings can be neither totally discounted nor conclusively linked to the most recent viral outbreaks in seal populations (22).
coral reefs The vibrant colors of tropical coral reefs are provided, in large measure, by zooxanthellae, algae living in symbiotic relationship with the coral and sponges that constitute the hulk of reef populations. Environmental stresses can cause this symbiosis to dissociate, turning the reefs white, a process known as bleaching. The actual mechanisms of dissociation are not well understood (231. Bleached corals are not dead, but their viability is greatly diminished. Bleaching is accompanied by increased vulnerability of corals to other stresses and can lead to mortality, reduced growth, and a loss of coral mass. Repeated bleaching events appear to undermine a reef’s ability to quickly reincorporate zooxanthellae and return to a fully productive condition (24). Glynn and de Weerdt (25)documented the elimination of two of 12 coral species from a Panamanian reef system after bleaching in the early 1980s; one of the species (Millepora sp. nov.) appears to have become extinct. Throughout the 1980s, coral reef bleaching was widely reported. Major bleaching complexes-a series of preliminary, localized bleachings followed by regional-scale eventsoccurred in 197-0, 1982-83, and 1986-88 (26);a fourth event began in 1990 in the western Atlantic and appears to be especially severe (27). The 198688 complex appears to be the best documented. Approximately 90 species bleached (chiefly coral, with a small number of sponges) in 35 countries a n d o r islands of the western North Atlantic, with additional bleachings reported in the Indian and Pacific Oceans
and in other reefs around the world. Virtually every identifiable species of coral i n t h e Caribbean had bleached, even in unusual species with nonphotosymbiotic algae or in coral hosting cyanobacteria rather than zooxanthellae. Many reefs bleached with such suddenness that the normally clear waters turned murky with expelled algae. The scale and severity of coral reef bleaching was widely viewed as surprising and without historical precedent. The global scope of the bleaching has been well documented. In several areas-Taiwan, for instance-bleaching had never before been reported. The 1987-88 Caribbean bleaching was considered the most severe and extensive ever recorded, as were 1987 bleachings in Australia, Maldives, Hawaii, Florida, and the Bahamas. In 1989, Jamaica experienced the most severe bleaching episode ever observed in that area. Massive coral reef bleaching in the Florida Keys is known to have occurred five times prior to 1980 (1911, 1914, 1958, 1966, and 1973) and three times since that date (1983, 1987, and 1989), and has extended much further north then previously recorded
1480 Ennmn. Sci. Technol., Vol. 26, No. 8. IS92
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A number of scientists have postulated that the principle cause of the bleaching events is a worldwide warming of ocean temperatures. Corals tolerate a relatively narrow temperature range. Although long-term temperature data are not broadly available for much of the affected waters, a general warming trend in recent decades (2) and long-term temperature data
from several affected reefs do point to increasing ocean water temperatures above levels easily tolerated by coral reefs. Global warming may be a contributing factor, one that elevates baseline ocean water temperatures around the globe, so that natural climatic and oceanic fluctuations (such as El Niiio warmings) can more readily raise temperatures above those tolerated by the reefs (Figure 2). The lack of reliable longterm temperature data for many of the affected areas makes it difficult to confirm this hypothesis, and few scientists appear ready to accept bleaching as a signal of global warming (28,29). In addition to bleaching complexes, coral reefs are also suffering from a condition known as white bend disease, apparently worldwide. The drastic decline of the coral species Acoropora spp. has been attributed to white band disease. The disease may be related to adverse environmental conditions, though its etiology is not well understood. The Great Barrier Reef and other Pacific reefs have been extensively affected by outbreaks of crown-of-thorns starfish, whose population growth may be spurred by abundant phytoplankton blooms as a result of eutrophic waters (30).
Sea urchins In terms of overall population impact, the decimation of the black sea urchin, first observed in 1983,is unparalleled amongst the MMEDs reported here. Once ubiquitous in the shallow waters of the Caribbean, the black sea urchin has virtually disappeared, its populations routinely re-
Resilience1
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duced to 1% or less of former densities i n little more than a year. Afflicted animals become lethargic, lose their spines, and die. An assessment of the population five years after the onset of the epizootic revealed that recovery was weak and sporadic: the ultimate capacity of the population to survive is unknown (31). Recent observations suggest a renewed wave of the epizootic began in 1991, attacking the small percentage of animals left after earlier die-offs (32). The decline was likely due to an unidentified water-borne pathogen; Lessios has documented how the spread of mortalities followed (with some exceptions) prevailing Caribbean currents (31). There is still considerable uncertainty, however, as to what caused such a catastrophic and rapid decline, or whether pollution played a role. Mortality of another species of sea urchin, Strongylocentrotus drobachiensis, from a disease organism was highly temperature dependent; the disease caused the death of sea urchins only when water temperatures were at a maximum. Thus, there is a potential mechanism whereby general warmings (from n a t u r a l or p o l l u t a n t - i n d u c e d causes) can interact with disease organisms to result in increased mortalities. However, Lessios ( 3 1 ) found no correlation between elevated temperatures and black urchin die-offs. Scientists have also raised the question (2) of whether the decline of the sea urchins, an important grazing organism on coral reefs, may have contributed to overall stress of the coral reefs, increasing their susceptibility to other sources of stress such as those leading to bleaching complexes.
fish populations i n the United States and Canada: these have been well documented by Harshbarger and his colleagues (34). Of the documented tumor epizootics in North American fish, more than half involve liver neoplasms. More so than any other tumor type, liver tumors appear to be associated with pollution: they are prevalent in fish populations in polluted waters and are readily induced in the laboratory by exposure to chemical pollutants, but are rare in wild fish populations in pristine waters and in experimental control populations. Other epithelial neoplasms also seem to be strongly correlated with exposure to certain pollutants and rarely occur otherwise. The bulk of the epizootics of fish tumors has been observed in the Great Lakes area and along the northeastern US.coast, both highly industrialized areas with abundant examples of extremely polluted waterways (Figure 3). Most of the observations have been in fish sampled from fresh water, although the observations include fish from Chesapeake Bay, Narragansett Bay, Long island Sound and other salt water bodies on the East Coast, as well as episodes that occurred in Vancouver Harbor, California coastal waters, the Gulf of Mexico, and Puget Sound. Epizootics of liver tumors most often occur in bottom-dwelling species of fish, presumably an effect of feeding patterns and of close associ-
ation with contaminated sediments. Epidemiological studies, experimental carcinogenesis, and metabolic considerations all point to polycyclic aromatic hydrocarbons (PAHs) as a key pollutant involved in tumorigenesis. Hawkins et al. (35) demonstrated that even brief exposures to moderate (50 ppb) or high (150 ppb) concentrations of PAH-contaminated solution could induce tumors in fish; 19% of guppies briefly exposed to moderate concentrations and 46% exposed to high concentrations developed'tumors after 37 weeks. Myers et al. (36) demonstrated a positive statistical association in English sole between the presence of aromatic hydrocarbon contamination i n sediment samples and the prevalence of liver neoplasms. Other chemicals, including PCBs and other chlorinated organics, have also been implicated as tumorinducing substances, although the field and laboratory data is not as complete as for PAH compounds. These epizootics may be global in scope, appearing limited to certain areas only because the geographical scope of scientific investigation has been limited (M. Myers, personal communication, June 19, 1991). However, surveys of highly polluted waters of the Sava, Rhine, and Elbe Rivers in Europe and of Port Phillip Bay in Australia failed to find fish neoplasms common at these sites (37). It is well recognized that incidences of fish neoplasms can arise
Fish tumors Neoplasms in fish have been reported since the mid-19th century. By the early 1960% a number of comprehensive studies had identified a variety of isolated neoplasms as well as apparent epizootic cancers in fish populations limited largely to three main types: epidermal papilloma, lymphoma, and peripheral nerve sheath cell tumors. Dawe et al. [33)reported the first incidence of liver cancer in wild fish populations, in white sucker and brown bullhead from a lake i n Maryland. For the first time, the researchers suggested that pollutants might be the cause. In the intervening years, more than 40 tumor epizootics have been identified in wild Environ. sci. Technol.. Vol. 26. NO. 8. 1992 1481
from natural causes, especially viral infection. However, Harshbarger and Clark (34) have laid out the following useful framework for distinguishing pollution-related liver neoplasms from naturally occurring events: History. An epizootic liver neoplasm was first discovered in fish in 1964, coincident with the postWorld War I1 exponential growth of the synthetic chemical industry and consequent pollution. Prior to this time, this type of tumor had not been observed, despite fairly extensive observations. The second such neoplasm in fish populations was not observed until 1975, but they have become frequent since then. Physiology. Fish livers contain enzymes capable of metabolizing some synthetic chemicals to reactive electrophillic metabolites capable of inducing tumors. Experiments with pure compounds. Virtually all of the known carcinogens tested on fish species have produced liver cancers. Tumors have also been induced at other sites, but with less regularity than in the liver. Experiments with field contaminants. Exposures to contaminated sediments or sediment extracts resulted in liver and other tumor formations in numerous fish species and in mice. The tumors induced in the laboratory often resembled lesions observed in the field. Spontaneous liver neoplasms. Liver tumors in fish are exceedingly rare in populations from unpolluted waters, or from control populations in laboratory experiments. Furthermore, deactivation of a coking plant in one river was followed by a decline in the presence and severity of liver tumors. Myers et al. (36) also point out the apparent absence of any evidence of viral etiologies for the epizootic of liver neoplasms in English sole. Extinct and threatened fish There are other indications of fish populations under stress, at least some of which are associated with pollution. Although habitat alteration (e.g., water diversions) and introduced species are major causes of fish population declines, pollution plays a significant role. Of the 40 known extinctions of freshwater fish in North America since 1900, pollution was a primary or contributing factor in 38% of the cases (38) 1482 Environ. Sci. Technol., Vol. 26, No. 8,1992
No one type of pollution dominated; reports range from agricultural, industrial, and urban runoff, to sewage discharge from a hot springs resort, to deliberate poisoning with ichthyocides. A review of North American freshwater fishes considered endangered, threatened, or of special concern (39) concluded that the health of aquatic habitats has decayed in the past decade. Acid rain is one of a number of important contributors to that decline, affecting more than 100,000 lakes in Ontario and Quebec. Although acid rain may not always lead to fish population loss, acidification has destroyed all wild stocks of the aurora trout and has eliminated half the range of the Acadian whitefish. A survey of 1000 lakes in southern Norway revealed widespread loss of fish populations from acidification (40).The number of barren lakes doubled since the early 1970s so that 64% of the lakes surveyed cannot support fish life; only 10% of the lakes contain fish populations apparently unaffected by acidification. In the United States, it has been estimated that acidification (from both natural and anthropogenic origins) has led to the loss of acid-sensitive fish populations in 20% of the lakes in the Adirondacks, 30% of streams in the mid-Atlantic highlands, and 60% of streams in the mid-Atlantic coastal plain (42). Acid rain has also been linked to high concentrations of mercury in fish in the United States, Canada, and Scandinavia at levels considered unsafe for human consumption. Lowered pH facilitates bacterially m e d i a t e d methylation of mercury, making the metal bioavailable to fish (42).However, mercury pollution is by no means restricted to acidified waters. A survey of pollutants in fish in 314 U.S. sites (43) revealed mercury, PCBs, and DDTmetabolites in more than 90% of all fish sampled; maximum concentrations were 1800, 124,000, and 14,000 ppb, respectively. It should be noted, however, that a review of causes of freshwater fish declines in California found pollution to be only a minor factor (44). Pollution appears to be linked to fish diseases other than cancers. A study of commercial fish catches from Biscayne Bay, Florida, revealed a high incidence of diseases and abnormalities, particularly among bottom-feeders. In many catches of striped mullet and Atlantic croaker, every individual was
diseased. Abnormalities were common in polluted waters and less frequent elsewhere (45). Heavy pollution of Hangzhou Bay (China) is thought to be partly responsible for a decline of 50% in the annual fish catch (46). Phytoplankton A number of scientists have noted fairly dramatic changes in the phenomenon of near-shore phytoplankton blooms in many locations around the globe. The quantity and extent of such blooms is increasing, and many organisms not known to have bloomed in the past, or not indigenous to a particular area, are suddenly blooming with unexpected frequency and in unusual locations. Bloom conditions have increased in the Baltic Sea, Kattegat (strait), Skagerrak (arm of the North Sea), Dutch Wadden Sea, North Sea, Black Sea, Tolo Harbor (Hong Kong), and the Seto Inland Sea in Japan ( 4 7 ) , along the eastern U.S. coast ( 4 8 ) ,the Gulf of Thailand (49) and in the Adriatic Sea ( 5 0 ) . In many instances, anthropogenic enrichment of nitrogen and phosphorous has led to increases in the ratios of these nutrients relative to silicon; this increase has been a key factor in both the increase in blooms and the frequency of novel blooms, generally favoring blooms of nondiatom organisms. Tolo Harbor, for instance, which routinely experienced one or two red tide blooms per year in the 1970s, now routinely reports 16-20 blooms per year, and had a record 39 blooms in 1988 (52). The increase was mirrored by a sixfold increase in human population and a 2.5-fold increase in nutrient loading to the harbor. Red tide blooms in the Set0 Inland Sea increased from 44 per year in 1965 to 326 per year in 1976, accompanied by a doubling in nutrient enrichment. Pollution controls instituted in the mid-1970s reduced nutrient loading, and bloom events fell sharply to about half of their peak levels (Figure 4). A brown tide episode along the northeastern U.S. coast in 1985 is representative of the unusual nature of many recent blooms ( 4 8 ) . A dense bloom first noted in Great South Bay, Long Island, NY, in spring 1985 turned the waters a muddy brown. Aerial and surface water observations confirmed a widespread bloom, highly unusual in three aspects: the suddenness of its appearance; the extent of the
Goodwin, M. H.; Sanders. A. E. Written testimony to the United States House of Representatives Committee on Merchant Marine and Fisheries Hearing on Mass Mortality of Bottlenose Dolphins. May 9-10, 1989, pp. 17-9.
Geraci, J. R. Oral testimony to the US. House of Representatives Committm on Merchant Marine and Fisheries Hearing on Mass Mortality of Bottlenosethdphins,May 9-10,1989.p. 61. Beland, P.Oral testimony to the US. House of Representatives Committee on Merchant Marine and Fisheries Hearing on Mass Mortality of Bottlenose Dolphins, May 9-10. 1989, pp. 38-40.
Greenpeace 1989,Written testimony to the U.S. House of Representatives Committee on Merchant Marine and Fisheries Hearing on Mass Mortality of Bottlenose Dolphins, May 9-10, 1989,113-32.
Martineau. D. Oral testimonv to the U.S. HO& of Representatives committee on Merchant Marine and Fisheries Hearing on Mass Mortality of Bottlenose Dolphins, May 9-10. 1989, pp. 4 4 4 6 . (9) Smayda, T. Oral testimony to the US. House of Representatives Committee on Merchant Marine and Fisheries Hearing on Mass Mortality of Bottlenose Dolphins, May 9-10, 1989,pp. ..
bloom, extending from Rhode Island south to New Jersey; and the bloom organism, a previously unknown nannoplankton, eventually classified as A u r e o c o c c u s anophagefferens. The bloom may be striking in another feature as well its persistence. Some bays along the east coast were still afflicted with the bloom well into 1990. The bloom organism, for reasons that remain unclear, could not support shellfish and starved much of the scallop and mussel populations along the affected coasts. The bloom also turned the water extremely opaque, limiting light penetration and photosynthesis. Significant areas were depleted of eelgrass populations (an important nursery area for finfish and shellfish) due to the reduced light penetration. Researchers examining the nutritional needs of A. anophageggerens have made a preliminary and, if c o n h e d , ironic finding on a contributing cause to the massive bloom. The bloom organisms grow especially well with additions of citrates to laboratory cultures; citrates, chelating agents, may in fact be acting as a limiting nutrient. Citrates are added to some detergents as a replacement for phosphates, which are an environmental concern and have been banned in some areas. The detergent additives may be a significant source of citrates in coastal waters. A large section of the Scandinav i a n coastline h a s also been plagued by troublesome and highly unusual blooms in recent years. For instance, Chry.sochromulina polylepis, never before reported as a bloom organism in the affected waters, created a massive bloom along
the Scandinavian coast in 1988.The bloom was also unusual in that the organism, known to bloom elsewhere, was never before reported to produce toxic blooms. The Scandinavian bloom released a biotoxin which, along with oxygen depletion, resulted in mass mortalities of 33-38. marine animals and seaweeds (5.21. One hypothesis for the C. polylepis (10) FitzGerald, L. M. S w Frontiers 1991, March-April, 50. blooms is that the destruction to (111 The New York Times, October 28, Scandinavian forests caused by acid 1990,p. 3. rain is resulting in an observed in- (12) The New York Times, September 4, crease of about 3% per year in the 1991,p. A4. quantity of humic material washed into coastal waters. The changing nature of nutrient loading, in turn, is spurring the growth of unusual species of phytoplankton. Blooms may also be affected by toxic chemicals due to differential responses amongst species. Laboratory experiments (53)have shown that exposure of Chesapeake Bay algal populations to copper favored the growth of a diatom and bluegreen algae over other species: arsenic favored the growth of an unidentified species of nannoplankton. David Snmkin is o biologist with the Contaminantsin coastal waters may U.S. Environmental Protection Agency. be an additional factor contributing His M.S.degree isfmm the Stote Univerto phytoplankton successions re- isty of New York a t Stonybrook. sulting in monospecific blooms. The views in this article are those of the authors and not necessarily of the institutions with which they are affiliated.
References (1) Laycock, G. Audubon 1990,May. (2)
Williams, E. H.; Bunkley-Williams, L. Atoll Research Bulletin 1980, 335,
1-71. (3) Scott, G. P.: Burn, D. M.; Hansen, L. J. Pmc. Oceans '88 [Baltimore, MD), 1988,819-23.
Jay Schulkin is a n Assistant Professor of Behavioml Neuroscience at the University of Pennsylvania. His Ph.D. is fmm the University of Pennsylvania.
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(13) “Marine Mammal Strandings in the United States”; U.S. Dept. of Commerce; U.S. Government Printing Office: Washington, DC, 1990; NOAA Tech. Report NMFS 98. (14) Aguilar, A. Preliminary Report on the Epizootic of Mediterranean Dolphins, University of Barcelona, 1990. (15) Cockcroft, V. G. et al. S . Afr. I. Mar. Sci. 1989, 8, 207-17. (16) Dietz, R. et al. Ambio 1989, 1 8 ( 5 ) , 2 58-64. (17) Visser, I.K.G. et al. Arch. Virol. 1990, 111,149-64, (18) Dietz, R.; Ansen, C. T. Nature 1989, 338, 627. (19) Osterhaus, A.D.M.E.; Vedder, E. J. Ambio 1989, 18(5),297-98. (20) Dickson, D. Science 1988,242,893-95. (21) Zakharov, V. M.; Yablokov, A. V. A m bio 1990, 19, 266-69. (22) Stolzenbeurg, W. Sci. News, August 11, 1990. p. 84. (23) Hayes, R. L. Oral testimony to the US. Senate Committee on Commerce, Science and Transportation, Hearings on Coral Bleaching, Oct. 11, 1990, pp. 4-8. (24) Wicklund, R. I. Oral testimony to the U.S. Senate Committee on Commerce, Science and Transportation, Hearings on Coral Bleaching, Oct. 11, 1990, pp. 14-16. (25) Glynn, P. W.; de Weerdt, W. H. Science 1991,253, 69-71. (26) Williams, E. H. Oral testimony to the U.S. Senate Committee on Commerce, Science and Transportation, Hearings
on Coral Bleaching, Oct. 11,1990,pp. 16-19. (27) Williams, E. H. Testimony to the U S . House of Representatives Committee on Energy and Commerce, Subcommittee on Health and the Environment, February 21, 1991 (in press). (28) Roberts, L. Science 1991, 253, 258-59. (29) “National Science Foundation Workshop on Coral Bleaching, Coral Reef Ecosystems and Global Change: Report of Proceedings”; Maryland Sea Grant College, College Park, MD, 1991. (30) Brodie, J. E. et al. “State of the Marine Environment i n the South Pacific Region’’; United Nations Environment Program: New York, 1990; UNEP Regional Seas Reports and Studies No. 127. (31) Lessios, H. A. Ann. Rev. Ecol. Sys. 1988, 29,371-93. (32) The Washington Post, August 11, 1991, p. A4. (33) Dawe, C. J.; Stanton, M. F.; Schwartz, F. J, CancerRes. 1964,24,1194-1201. (34) Harshbarger, J. C.; Clark, J. B. Sci. Total Environ. 1990, 94, 1-32. (35) Hawkins, W. E. et al. Sci. Total Environ. 1990, 94, 155-67. (36) Myers, M. et al. Environ. Health Perspect. 1991, 90, 7-15. (37) “Preface”; Sci. Total Environ. 1990, 94, ix-xi. (38) Miller, R. R.; Williams, J. D.; Williams, J. E. Fisheries 1989, 14(6),22-40,
BIOREMEDIATION 021C02 Respirometer
(39) Williams, J. E. et al. Fisheries 1989, 14(6),2-20. (40) Rosseland, B. 0.; Henriksen, A. Sci. Total Environ. 1990, 96, 45-56. (41) “National Acid Precipitation Assessment Program Integrated Assessment: Questions 1 and 2”; External review draft, August 1990. (42) Raloff, J. Sci. News 1991, 139, 152-56. (43) “Bioaccumulation of Selected Pollutants i n Fish”; U.S. Environmental Protection Agency. US. Government Printing Office: Washington, DC, April 1991; draft EPA 506/6-90/001a. (44) Moyle, P.; Williams, J. E. Conserv. Biol. 1990, 4, 275-84. (45) Skinner, R.; Kandrashoff, W. Water Resour. Bull. 1988, 24, 961-66. (46) Liu, P.; Yu, Y.; Liu, C. Mar. Pollut. Bull. 1990, 23, 281-88. (47) Smayda, T. In Toxic Marine Phytoplankton; Granelli, E. et al., Eds.; Elsevier: New York, 1990. (48) Bell, T. Sea Frontiers 1989, JulyAugust, 239-45. (49) Suvapepun, S. Mar. Pollut. Bull. 1991,23, 213-17. (50) Vukadin, I. Mar. Pollut. Bull. 1991, 22,145-48. (51) Environment Hong Kong 1991: A Review of 1990; Environmental Protection Department of Hong Kong. (52) Underdal, B. et al. Ambio 1989, 18, 265-70. (53) Leffler, M. Marine Notes; Maryland Sea Grant College, College Park, MD, January 1991.
Request for Letters of Interest and Qualifications for Treatment of Fly Ash from a Municipal Solid Waste Incinerator The Greater Vancouver Sewerage and Drainage District (GVS&DD), a division of the Greater Vancouver Regional District, hereby invites letters of Interest and Qualifications from wmpaniesquallfied to treat fly ash and lime residues captured in the air pollutionwntrol equipment of a municipal solid waste incinerator. The fly ash is considereda Special Waste (hazardous waste) under British Columbia legislation due to the quantity of lead which leaches when the material is subjected to an acM leachate extraction procedure.
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c1 Measures 0, and C02 consumption/production in 1 to 80 measuring chambers using a single set of sensors (periodically measures headspace gas concentrations). c1 Temperature of samples can vary during experiment. c1 Allows removal of sample substance from inside of the chambers during experiment. Q Superior sensitivity 0.2plh Important for low level biological activity. D Measuring chambers can be user’s own, 50ml to 10 L. D Real time graphics, fully computerized. Q Measures both liquids or solids. Q Programmable air refresh, 24 hour operation. COLUMBUS INSTR TERNATIONAL PH:(614)
276-0861
0 4 3 2 0 4 USA 16-0529 TLX: 246514 -
CIRCLE 1 ON READER SERVICE CARD
1484 Environ. Sci. Technoi., Vol. 26, No. 8, 1992
Approximately 8,000tonnes/year of the material is produced of which 33 37% is spent lime. Treatment or processing must render the material anonSpecial Waste to the satisfaction of the British Columbia Minlstry of Environment, Lands and Parks and sultabie for utilization or conventional landfill disposal. Approxlmateiy 35,000 tonnes of materlai in temporary storage in a monofiii also require treatment. At thls stage, the District’s objective is to assemble a short-list of companles representing various technoiogieswithdemonstrat~expertise and success in treating material of thistype. Theshort-iistedcompaniesmay beinvitedtopreparefuii proposals should the GVRD decide to undertake the work. Requests for copies of background Information on this project are to be directed to: Greater Vancouver Regional District Purchasing Department 5th Floor, 4330 K i n g s w y Burnaby, B.C. Canada V5H 408 Telephone: (604)432-6326
Greater VanCOUW Rqgional District
BY
To receive consideration, companies must present their Letters of interest and Qualifications, including references, to the attention of Purchasing Department,GVRDattheaboveaddress. RequestsforadditionalInformation regardingthismattermay bemade bycalllng Mr.MikeStringerat(604)436. 681 0 . Fax: (604) 436-6811 . R.J. Lalonde Purchasing Manager ~~
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CIRCLE 7-ON
READER SERVICE
CARD
