Bleached Kraft Mill Effluent and this Planet
Kraft Mill Effluent and this Planet: PCB’s, Mercury, Dioxins, Furans and other (POP) Contaminants in Bleached Kraft Mill Effluent (BKME), Receiving waters, Fish, Wildlife and Humans, with Emphasis on those that are Cancer Causing.
By Jorma Jyrkkanen, BSc, P.D.P., Environmental Biologist
Contact Me 250-859-533012 April, 1989
This is background material for a slide show and report given at a televised forum in Quesnel, hosted by Quesnel and District Citizens for a Clean Environment, 22 March, 1989 which addresses pulp mill pollution issues and discusses solution.
Contents Page
Introduction
Bleached Kraft Mill Effluent (BKME)
Trace inorganic contaminants
Fatty, aromatic and resin acids
Phenols and chlorinated phenols
Volatile organohalides
PCB’s and organochlorine pesticides
Trace contaminants
PCB’s and the Aquatic ecosystem
Fish contamination by PCB’s
Mercury in the environment
Dioxins and furans in the west coast fishery
Relative toxicities of PCDD and PCDF isomers
Salmonid dioxins and furans/20 ppt limit
Fish toxicity of dioxins and furans
PCB’s and organochlorines in marine mammals
The Bald eagles of Ontario and Quebec
The Inuit PCB’s
Mothers Milk World-wide
Carcinogenic POP pesticides in mothers milk
Carcinogenic OC’s in BKME and Mom’s milk
Volumes of BKME, tonnage of OC’s
Conclusion
Introduction
In researching this issue, I tried to come to terms with the question of where pollutants ended up. Of course some goes into the air, some into the soil, some into the water and sediments and some into plants and animals and some into us humans.
Being particularly water pollution in this review as it pertains to bleached Kraft mill effluent (BKME), I chose to focus on the fate of pollutants in water and to follow their movements through the food chain.
The ensuing story is a somber eye opener regarding the extent and pervasiveness of deleterious substances and there are a few surprises for us all. It is also a story about human greed, past cover-ups and miss-information, and clearly points up the conflict government has had in pursuing its goals and the dreams of its backers.
It is a story made possible by crimes against nature and by secretly permitting violations of the laws of Canada, from the sincere belief that greater social good would come from sacrificing the health and habitability of planet earth for jobs.
For years, despite the warnings of environmentalist, the pervasive philosophy governing pollution was dilution, leading to taller smoke stacks and longer discharge pipes and ocean dumping.
Then problems arose like acid rain which has killed nine salmon rivers in eastern Canada, is rendering lakes and streams life-less world-wide and severely altering forest ecosystems and ozone depletion and uvb radiation, poisoning of the Oglala aquifer with pesticides, the Greenhouse effect, Three Mile Island, Windscale and Chernobyl.
These problems suggest that dilution is not a solution; that the geological sediment sink and chemical breakdown cannot keep pace with our waste stream discharges.
Despite the ramifications of this great experiment, driven by the philosophy that growth, profit and jobs come before all else, the escalation of which is permitted by Waste Management Agencies worldwide, we continue to treat nature as something else, apart from humankind. I will demonstrate that the chickens let go come home to roost.
We apparently fail to see that we are filters of nature, our very bodies completely built up of products of nature, because our social values set us apart from nature. In this our politicians, our educators, our scientists, our policy makers, have failed us bitterly.
Lets look at what is discharged in BKME.
Bleached Kraft Mill Effluent (BKME)
Christina Cherwinsky and Don Murray (1986) compiled a list of contaminants in pulp and paper mill effluents in Ontario. What they found was staggering.
The ratio of pollutants out in effluent to that at the intake is 10,000X (times) for reactive phenolics, 5000X for biological oxygen demand (BOD), 490X for chemical oxygen demand (COD), 300X for tannins, 250X for sodium, 140X for dissolved oxygen concentration (DOC), 80X for suspended solids, and 50X for color.
With one exception, high bacterial densities were found. These (the high densities) included heterotrophs, total coliforms (E. coli or Pseudomonas aurigenosa strains), sulfate reducers, fecal coliforms, fecal streptococci.
Trace Inorganic Contaminants
Carcinogenic trace inorganic contaminants included mercury, which methylates in receiving waters, bioaccumulates and becomes a Minimata’s disease hazard; arsenic, cadmium, chromium, nickel, lead, zinc (See IARC, 1986. Carcinogenic Metals).
Present was also iron, cobalt, copper, aluminum, and hydrogen sulfide which is incidentally linked to increased lung cancers in southern US studies (Hitchcock, R. 1979). Copper, iron, zinc, cadmium, and hydrogen sulfide were above the Provincial Water Quality Objectives for protection of aquatic life.
Fatty , Aromatic and Resin Acids
Fatty, aromatic and resin acids were high in almost all effluents examined. All have high acute fish toxicity and are found mostly in foam of effluents.
There was high variability between different dates of sampling at the same mills, ranging from none detected to 8066 ug/l or parts per billion (ppb). Pimaric, sandarachopimaric, isopimaric, and abietic acids were well above the reported lethal to 50% of fish over a 96 hr exposure at some mills tested.
Some of these acids have been listed as suspected carcinogens (oleic acid) or possible carcinogens (abietic, dehydroabietic, isopimaric, pimaric, sandarachopimaric, linoleic and linolic acids) (BC Research, 1979, Cited in Cherwinsky).
Abietic acid has been nominated to the NCI for carcinogenesis bioassay (Sigman et. al. 1984-In Cherwinsky).
Should these acids form alcohols, then capric, lauric, and oleic acid cis methyl ester and capric, dodecyl and myristic are all conclusive mouse skin carcinogens (Sax, I. 1981).
To be fair, I should point out that linoleic acid has been found to have anti-cancer activity and is also present in hamburger.
These acids can to a large extent be governed by In-Mill procedures and by post mill effluent treatment (Bonsor et. al. 1988).
Phenols and Chlorophenols
Phenols are natural compounds found in wood which offer some degree of protection from disease and are also involved in plant pigments. The are biotoxic and have been used in the past for antiseptic soaps.
Natural chlorination of them is rare but is the rule in Kraft mills, leading to chlorophenols, a much more toxic class of substances. These chlorophenols can lead to fish and water tainting as well as carcinogenic transformation.
In both classes, Cherwinsky found phenols, vanillin, homovanillic acid, guaiacol, acetovanillin, vanillic acid and acetosyringone. She also found the chlorophenols, dichlorophenol, trichlorophenol, tetrachlorophenol and pentachlorophenol.
The higher the number of chlorine atoms bound to the phenol, the more toxic it potentially becomes.
Chlorophenols are also converted into dioxins in low temperature regions of the furnace and especially where chloride salts are present. It is for this reason that burning pentachlorophenol treated wood in a campfire or fireplace is so dangerous.
Human exposure to chlorophenols has been linked to increased cancers (Hardell and Sandstrom, 1979; Ericksson et al. 1981; Hardell et al. 1981; Hardell, Bo Johansson and Olav Axelson, 19812 (Cited in IARC Monograph vol. 41 and prior) and most significantly because it is directly associated with my discussion, in the pulp and paper industry, to significantly elevated reticulosarcomas and lymphosarcomas (Gallagher, 1986).
Guaiacol was high enough (>100 ug/l) to cause fish tainting in some effluents while phenol was found in 3/9 mills sampled with levels below tainting levels (<5600 ug/l). A few effluents had tetrachlorophenols above surface water guidelines of 1000 ng/l or parts per trillion (ppt). A number of mill effluents were in exceedence of the 400 ng/l PCP limit of the Great Lakes Water Quality Agreement (GLWQA).
Oikari (1986) [in Bonsor, 1988] found an accumulation of the following chlorinated organics at levels above 1000 ug/ml (ppm) in fish tissue near pulp mills: 2,4,6-trichlorophenol; 4,5,6-trichloroguaiacol; 3,4,5,6-tetrachloroguaiacol; pentachlorophenol. Clearly the ability of these substances to bioaccumulate is significant.
The 2,4,5-trichlorophenol (2,4,5-TCP) is a precursor to 2,3,7,8-TCDD, the infamous most deadly dioxin which is found in virtually all Kraft mills (Bonsor, 1988). While Cherwinsky found no 2,4,5-TCP at the limits of detection at 50 ppt, it must have been present because this dioxin was found, or perhaps some other process was generating this isomer. You may recall that 2,4,5-T, the phenoxyacetic acid variant, was one ingredient in Agent Orange.
Volatile Organohalides
Chloroform was found in 7/9 mills sampled at levels up to 4036 ug/l.
Chloroform is a confirmed animal kidney and liver carcinogen (Sax, 1981; BC Research 1979; DHHS, 1981) and a suspected human carcinogen (ACGIH 1984. Group 2B carcinogen in IARC Monographs, Oct. 1982).
Chloroform caused dose-dependent pre-neoplastic liver foci in rats (Deml, E., Oesterle, D. Oct. 1985) and cancers of the liver and kidneys of mice and rats (Savage, R. E. et al. 1982).
Tetrachloroethylene, a conclusive liver carcinogen (Sax, 1981) and dichlorodibromomethane were found at around 10 ug/l on a few occasions. Both carcinogens may be due to water chlorination or chloramination since they or close relatives may also be found in drinking water across Canada.
PCB’s and Pesticides are Produced by Kraft Process
Organochlorine pesticides were detected above the limits of detection (1-5 ng/l) and these included alpha, beta, gamma isomers of benzenehexachloride (BHC or hexachlorocyclohexane), [oral-mouse-conclusive carcinogen, animal-positive-carcinogen-IARC]; gamma-chlordane [concl-mouse-liver-carcinogen-IARC supplement 4, Oct 1982. P. 81]; dieldrin; hexachlorobenzene (HCB), [oral-hamster-conclusive; parathyroid adenomas and phaeochromocytomas in male and female rats with additional neoplastic liver nodules in females (Arnold, D.L. et. al. 1985].
The above were detected among 21 organochlorines (OC’s) screened. Others can be inferred from the above findings. For example: aldrin which is a precursor to the more persistent dieldrin and only needs to be oxidized to become dieldrin.
While the OC’s were present at levels ranging from less than 2 up to 24 ppt, it must be kept in mind that these have huge bioaccumulation factors and there are enormous volumes of effluent in the pulp and paper industry. Prince George BC produces many millions of cubic meters of effluent a year from my review.
Of the OC’s, PCB’s are the most interesting to me, because of what they tell about the whole story and because they have been the most extensively studied. I shall give evidence that they are more insidious than has been let on. We have been led to believe that they are in old transformers and that’s it. This is so wrong, it really needs the light of day.
All PCB samples detected exceeded the 1 ng/l Provincial Water Quality (PWQ) objectives for PCB’s. Actual dilution was 1:20 and to reach that objective it would require 1:2000.
It seems likely that considerable PCB’s are also deposited in pulp since the US FDA established 10 ug/g limits on PCB’s for food packaging in 1977 (US FDA, 1977a) and the highest levels of air and water PCB contamination in Japan were in the receiving environment of Recycled Paper Mills (Tatsukawa and Watanabe, 1972; Tatsukawa, 1976; Fukushima, 1974; (cited in IARC, 1978, Vol. 18).
Bonsor (April 1988) also states that, “We have avoided recommending a regulation on organochlorine content of pulp, since there is presently no proven technology available to control the split between pulp and effluent.” I give evidence later in the article that this is in fact true, thereby making chlorine bleached paper and BKME effluent bith serious offenders polluting the global environment with PCB’s, other OC’s, including dioxins and furans. Think about it. Paper is laced with OC’s and PCB’s. Next time your throw paper into a campfire and sit close inhaling smoke, think about what you have learned here.
These substances and other OC’s are known to affect the endocrine systems and reproduction (Helle, et al. 1976a; Allen et al. 1980; Olsson, M. et al. 1974) and immune system competency (IARC, 1978, vol. 18) among other effects.
I shall return to PCB’s later in the review because they deserve a fuller treatment along with mercury, dioxins and furans due to their omnipresence and toxicity.
Trace Contaminants
An enormous list of identified and unidentified trace contaminants was made by Cherwinsky.
Most of these chemicals could be found on list of chemicals of concern cross-referenced elsewhere. The potential for interaction effects and toxic degradation by-product intermediaries to be formed is enormous. While many of these are of concern, one stands out for me because it is representative and typical and its toxicology is well known, benzene, and it also forms much of the back-bone of Kraft process toxicology.
Benzene is known to cause acute myelogenous leukemia in humans (IARC Monographs, Vol 29. Pp:93-148).
I think that the reader will agree that a significant problem and an enormous challenge has been presented by these effluent findings. I wish to turn now to the aquatic environment and look specifically at the PCB contamination of that system globally.
PCB’s and the Aquatic Ecosystem
The following data come from IARC 1978, Vol 18. And I have cast them into a table See Table I.
Table I. PCB Levels found in the Aquatic Environment
Location Year(s) Levels (ng/l or ppt) Reference, Year USA, various 1971-74 100 to 3000 Dennis, 1976 Lk. Michigan, USA 1976 10 Klinert, 1976 Fuji, Japan, near recycled paper mill* 1973? 910 to 1200 Fukushima, 1974 Tokyo Bay, surface 1973 320 Fukushima, 1974 Ocean off Tokyo, at 20 m depth 3 ” ” ” “ ” ” ” “at 1500 m 0.5 ” ” ” “ Rhine River & Lk. Constance 1973-1975 Increased from 10 to 75 Eichner, 1976 Mediterranean, 11 locations 1975 13 Elder, 1976 Note: 0.38 ppq had irreversible effects on rainbow trout and led to over 38000X bioconcentration,
Mehrle et al. (1987). All these levels are in exceedence of 0.38 ppq (pg/l) in water.From these data, one would presume that pristine ocean had at most 0.5 ng/l and probably considerably less than this. By this standard, everywhere else now seems significantly contaminated. By the lowest level affecting rainbow trout all these waters are in exceedence.From Table I, it is clear that levels a Fuji could be as high as 2400 times those in the deeper oceans, and that these levels are associated with a recycled paper mill. Paper is thus an apparent source of PCB pollution specifically and by implication and inference from Bonsor’s statements about the impossibility of keeping this class of contaminants out of the pulp production, other OC’s as well. Re-Cycle Ricky would not be happy about this revelation.
Similar very elevated levels were found in the air over recycled paper mills ie. 12 ug/m3 versus 0.005 ug/m3 over medium sized cities, also a factor of 2400 times higher suggesting that paper and its production is the culprit and the repository of PCB’s.
There is also a generally elevated level of PCB’s in aquatic ecosystems associated most closely with drainages from heavily industrialized countries.
Fish Contamination by PCB’s, Mercury, Dioxins and FuransI firstly cast my available data into Table II.
Table II. Fish Contamination by Polychlorinated biphenyls (PCB’s).
Location Sample Year Levels (ug/g) Reference, Yr Japan, Marine Fish flesh 1972 1.0 in 16% SW Fujiwara, 75 ” “, Fresh Water ” “ 1972 1.0 in 18% FW ” ” ” “ ” “, polluted FW ” ” 1972 >3.0 ” ” ” “ Lake Michigan Trout 1972-74 12.9 to 22.9 Willford et al. 76 ” “ Coho 1972-74 10.4 to12.2 ” ” ” “ ” “ Bloaters 1972-74 5.2 to 5.7 ” ” ” “ Hudson River PCB Factory Shiners 78 Nadeau & Davis, 76 ” “ Rock Bass 350 ” “ Canada, Market Sample, marine 0.07 to 2.65 Graham, 76 ” “, Fresh W 0.1 to 17.14 ” “ Danube Lk, Hallstatt, Aus. 1973-75 0.1 to 0.3 Zislavsky, 1976 Swedish Fiord Livers 5.0 Falkmer et al., 78 ” “open sea Livers 0.2 ” “ The Swedish government bans fish that in excess of 5 ug/g so I have highlighted those fish in Red which would be banned if this standard were to be upheld around the world.The American standard is 2 ug/g (US FDA, 1977) for fish and I have italicized those that would be banned under this limit.
Were we to apply the Japanese PCB standard of a ban at above 0.5 ug/g, we would see the underlined fish and countries unable to sell fish. I recommend a new goal of 0.01 ug/g or 10 ppb for PCB’s in fish flesh as the maximum allowable limit.
Clearly, we already have a disagreement between our nations that if opting for the most strict Japanese 0.5 ug/g standard for health protection, would result in a ban on most fish products from this collection. We have therefore a serious problem with PCB’s, and either we deal with it by banning all these fish or issuing an advisory to restrict the number of meals whilst cleaning up the pollution mess in the receiving waters.
The problem for non-human piscivores is that they have no way of knowing which fish are over limit and they therefore are at serious risk. I have no doubt that this sort of thing is contributory to the collapse of the Atlantic Cod fishery in part. It also puts higher trophic level predators like marine mammals, sharks, scavengers, herons, eagles, fish eating birds of all sorts, and especially people who live by hunting and fishing and gathering outside the market economy, at extreme risk. I will deal with them later. Keep in mind also that PCB is just one indicator of OC contamination in general and the whole gamut of others is out there as well but not part of this survey. I now turn my attention to mercury levels in the environment. Please see Table III.
Table III. A Cursory Survey of Mercury (Hg) Levels in the Environment
Location Species Levels Reference, Yr Cda, unpolluted FW 0.1 ug/l-àppb Lake Ontario FW 0.39 ug/l Lake Ont. Effluent 3 to 4 ug/l Pinchi Lk BC, FW 0.32 ug/l BC F&W Br Unpolluted FW Fish 0.2 ppm Pulp Mill Downstream Pike 20 ppm;phenyl Hg acetate 10x-20x Gunnar et al,72 St. Clair Lk. Walleye 5.01 ppm Fimreite et al. St. Clair R. Pumpkinseed 7.09 ppm Pinchi Lk., BC, Old Hg mine Lake trout 10.5 ppm Lake Erie Fish 7.0 ppm Howe Sound BC Crabs 13.4 ppm Howe Sound Ling Cod 2.1 ppm ” ” Flounder/Rock fish 1.4 ppm ” “ Shrimp 2.75 ppm BC Coastal species Salmon/Steelhead/herring < 0. 5 ppm Cda, Edible Fish Std Edibility standard 0. 5 ppm World Health Org. Standard. Edibility for Fish 0. 05 ppm Cda too high by 10X Red necked grebe, Cda 17.4 ppm Tern eggs, 4 Cda 0.56 ppm Minimata’s disease if eaten Red breasted merganser 0.81 ppm Vanc. Island G. b. heron 50.0 ppm Gulf of Finland, unpoll Seal muscle 0.9 ppm Hendriksson, 68 ” ” , polluted Seal muscle 62.4 ppm ” “, unpolluted Seal liver 11.8 ppm ” “, polluted Seal liver 137.8 ppm Minimata’s disease Japan Human blood 1000 ng/g=ppb=1.0 ppm Japan, MOH, 67 Japan, unpolluted Human blood <15.2 ng/g=ppb Man/300gm/day/perchat 0.5 ppm Human whole blood 125 ng/g Birke et al, 72 Man/60 gm/day/” ” Human whole blood 27 ng/g Birke et al, 72 Bacteria are able to take metallic mercury and alkylate it into methyl and ethyl mercury which are much more toxic and then this form easily bioaccumulates up the food chain. The data in Table III clearly shows that the higher one goes up the food chain, the more contaminated an animal becomes.Table III also shows that fish in many lakes exceed edibility standards for the lax Canadian standard and many more exceed it for the World Health Organizations standard of 0.05 ppm. Canada’s unpolluted Fresh water fish mean of 0.2 ppm is above the WHO limit of 0.05 ppm so that Canada’s so called unpolluted fish would not be considered safe by WHO. Seals would be illegal and very dangerous to eat, but tell that to the Orcas and Polar bears and Sharks. The polluted areas are significantly above all standards for fish edibility.
Pulp mill pollution which can have as much as 17x the intake levels of mercury in the effluent must therefore be considered as being contributory to mercury pollution of fish and wildlife and human consumers. In Canada, there is the well known example of the Reed Pulp and Paper company polluting the English Wabigoon river system and inducing Minimata’s like symptoms in the Aboriginal populations at White Dog and Grassy Narrows reserves. This area had a spate of homicides unequalled in Canada to my knowledge. Uncontrollable outbursts of violence was one of the symptoms of Minimata’s disease, as were severe brain damage in offspring, local birds and cats.
I have conducted a mercury survey of chlor-alkali workers hair, urine and blood. The maximum blood level was 33 ppb and a control was 2 ppb. The reader can view the results at: http://www.geocities.com/jormabio/archive/restricted_hg_lvls.html
I was informed by a Minimata’s Society member from Japan, that daily consumption of 0.35 ppm in fish flesh can lead to Minimata’s disease. It is therefore imperative that Canadian’s be aware that many fish from our waters can potentially cause this condition if too many are consumed. If you are a large fish eater, it is important to have them sampled and tested periodically and to keep the total number of meals limited accordingly.
I recall that tuna is at 0.5 ppm so that a daily diet of only this fish would lead to Minimata’s disease. I have confirmation that it apparently does in cats. A friend fed her cat only tune and it went mad and ran of screaming into the forest never to return (Marie Payton, pers. comm. 1980)
Pregnant women should not eat Fresh water fish from Canada, and keep the number of such meals even when not pregnant to very low levels until we get these levels down. I recommend adopting the WHO mercury guideline for Canada to protect human health and animal health better for a period of ten years after which it should be reduced again by a factor of 10. This guideline should also be a target for our clean-up efforts.
All fish consumed in rivers with mills should be sampled regularly, before consumption. However, what to test for is still an open question. There are so many pollutants to worry about, from this investigator’s assessment.
Dioxins and Furans in the West Coast Fishery
Health and Welfare Canada Food Protection Branch, has set a limit for sport caught Canadian fish of 20 pg/g = 20 ppt for 2,3,7,8-TCDD, the deadly dioxin, in fish flesh.For regular consumers of fish, this level is too high. The maximum recommended daily intake (MDI) of 2,3,7,8-TCDD or its equivalent for a 90 kg person is 900 pg prior to dioxin being reclassified into a Class 1 human carcinogen. One only needs to eat 900/20 = 45 grams of fish at 20 pg/g to be at the limit. Because a normal meal may be as high as 200 to 300 grams, this would lead to 4000 to 6000 pg daily intake meaning that to stay within the 900 pg MDI one should conservatively set the limit for sport caught fish at < 3.0 ppt.
I know I have eaten considerably more than both these figures on many occasions. Native fishermen and their families and zealous sport fishers or those that are trapping or prospecting and living off local fish are potentially at risk.
The problem for Fishery Officers and Health officials is how to decide if the fish are over limit when combinations of the 75 other dioxin isomers are present in varying amounts, and concentrations of the 135 furan isomers are also present. What is the arithmetic of health protection or is there a simpler more practical way to get to the same place.
Fortunately, from the health of the consumer perspective, relative toxicities for the various isomers have been worked out based on the no-effect-levels (NOELS) for cancer, again prior to its revision as a Class 1 human carcinogen by IARC, at I believe what was thought to be 10-6 risk levels. These can be further lumped into similar toxicity groupings based on the number of chlorine atoms per isomer (Ont. Ministry of Environment, 1985) and I have used this information to construct the table below (Table IV).
One does this by converting the non-2,3,7,8-TCDD isomers of dioxins and furans into TCDD equivalents, by multiplying their concentrations by their relative toxicities and then summing the total to get the TCDDEQ loading. I will show how to use the total TCDDEQ method with an example employing Chehalis chinook data from DFO.
Data: 2,3,7,8-TCDD=6 ppt; H6CDD=18 ppt; 2,3,7,8-TCDF=69 ppt
Rel Tox 1 0.1 0.5 Computation:
TCDDEQ = [(TCDD)(Rel tox TCDD) + (H6CDD)(Rel tox H6CDD) +(T4CDF)(Rel tox T4CDF)]
= [((6)(1)) + ((18)(0.1)) + ((69)(0.5))] = 42.3 ppt
Note: This is 22.3 ppt over limit with aggregate dioxins and furans.
Another way is to compute the TCDDEQ for any single isomer and see if the limit has been exceeded.
For example, P5CDD is 0.1 times as toxic as TCDD, so one would need ten times as much for a limit, so that the limit for P5CDD would be 10 x 20 ppt = 200 ppt or pg/g. A fish at 350 ppt, would then be 150 ppt over limit.
Another example, P5CDF is 0.5 times as toxic as TCDD so that one would need 2 times as much to be in exceedence or 2 x 20 ppt = 40 ppt. A fish at 32 would therefore be 8 ppt under limit.
Table IV. Relative Toxicities of Dioxin and Furan Isomers
Isomer Group Toxicity Factor My Concern Level Dioxins M1CDD 0.0001 X D2CDD 0.001 XX T3CDD 0.01 XXX T4CDD* 0.01 XXX P5CDD 0.1 XXXX H6CDD 0.1 XXXX H7CDD 0.01 XXX O8CDD 0.0001 X * Excludes 2,3,7,8-TCDD Furans M1CDF 0.0001 X D2CDF 0.0001 X T3CDF 0.01 XXX T4CDF 0.5 XXXXX P5CDF 0.5 XXXXX H6CDF 0.1 XXXX H7CDF 0.01 XXX O8CDF 0.0001 X See MOE, Ontario, 1975, Table 3.6.7c
When I applied this method well rationalized but in error on the carcinogencity of TCDD, in the MOE Scientific Criteria Document to the West Coast fishery, I found that a number of open fisheries were over the old limit and should have been closed. I will give a few examples in detail.Gold river mussels had 341 ppt T4CDF which by virtue of this isomer being 0.5 times as toxic, should have an exceedence limit of 2 x 20 = 40 ppt. Clearly they are over and gold river mussels should be closed by the ld standard.
Victoria crabs are another dandy with 80 ppt TCDD, 313 PCDD, 1514 H6CDD, 225 H7CDD, 33 OCDD, 239 TCDF, 316 PCDF, 718 H6CDF, 205 H7CDF, 4 OCDF in their hepatopancreas. This amounts to [(80)(.01) + (313)(0.1) + (1514)(0.1) + (225)(.01) + (33)(.0001) + (239)(0.5) + (316)(0.5) +(718)(0.1) + (205)(0.01) + (4)(0.0001)] = 534.8 ppt TCDDEQ, just a wee bit over the 20 ppt limit. Clearly this fishery should have been closed by the old standard.
However, the old standard does not protect society adequately and it must be brought into line with the TCDD reclassification. I have considered this and make a recommendation below.
I encourage the Fishery Minister to recalculate their Canada wide findings and to close those fisheries which are in exceedence of the TCDDEQ loadings. However, I urge the Minister to change the Maximum Allowable Limit of TCDDEQ in fish flesh to 0.3 ppt to put a ten times safety factor on the ADI. I also encourage the Minister to enforce the fisheries Act fish habitat provision pertaining to dioxins and furans, mercury and PCB’s as required by the laws of Canada.
The situation is clearly far worse than we have been led to believe by the closure of only the Howe Sound and Prince Rupert shellfish fisheries.
Salmonid Dioxins and Furans in Relation to the TCDDEQ Limit
I have cast the 1988 DFO data into Table V and sorted these into TCDDEQ’s using the total load method.
Table V. Salmonid Dioxin and Furan Toxicities Loading of TCDDEQ
Dioxin or Furan Isomer (ppt) Species Location Age TCDD H6CDD TCDF P5CDF TCDDEQ Ch Quesnel Imm 68 28 375 12 264.3 Ch Chehalis Ad 6 18 69 42.3 Ch Pt Mellon Imm 19 24 11 14 33.9 Ch Morse Basin Ad 4 20 51 31.5 Ch S PG Imm 7 45 29.5 Ch Pt Mellon Imm 10 17 9 23 Ch Chehalis Ad 27 13.5 Sk Fraser Ad 19 9.5 Sk Stellako Ad 9 4.5 Sk Stellako Ad 8 4 Sk Stellako Ad 2 2 Ch Chat. Sound Ad 3 1.5 Ch Quesnel Imm 3 1.5 Pk Fraser Ad 0 Ch Pr. George Imm 0 Ch Port Alberni Ad 0 Note: Fish in red are in exceedence of my 0.3 ppt TCDDEQ in flesh.
Using this method it is easy to see that all these fisheries should be closed until remediation action has cleaned up the system. Using this method, it is also easy to see that the chinook immatures downstream of Quesnel are at most risk of dioxin and furan (and by implication of other OC’s presence) poisoning and consumers are at risk if they eat these fish on a daily basis.If it is harmful to chinook, it must be far worse for steelhead and coho and resident species which spend relatively much more of their lives in polluted waters than do chinook. Adult chinook at Chehalis might have picked up a lead by feeding in pulp mill basins. Herring seem to behave erratically near mills possibly due to intoxication (Lefty Goldsmith, pers. comm. 1978) and it is possible that this attracts chinook to feed near mills thereby exposing them to toxins. It is well known that Washington chinook feed in winter in Canadian fiords such as the Kitimat Arm so one should really look at them for this kind of exposure in returning spawners in Washington.
It is highly unlikely that juvenile fish contaminated as they move down river along the Fraser will ever return alive as adults since this contamination would seriously affect their probability of survival. They may not make it much past the smolt stage.
Thus, specific chinook stocks are more at risk than others through exposures while feeding in coastal areas affected by mill pollution.
Another important conclusion is that TCDF appears to be more of a culprit at more locations suggesting that it is perhaps more easily picked up or is present at higher levels in the environment.
It seems prudent at this time to turn to the toxicology of dioxins and furans on fish to determine how anadromous and other stocks should be protected from these pollutants. The question is, should we be managing for 20 or 0.3 ppt sport fish edibility limit or for the survival of the stocks or for some other limit?
Toxicology of Dioxins and Furans in Fish
Halder (1980, 1981) studying rainbow trout (Rb) and pike eggs exposed for 96 hours water exposure and 163 days of observations, found effects ranging from retarded embryonic development and growth at 0.1 ppt, while there were skeletal malformations, liver, stomach and pancreas damage at 100 ppt. This argues for levels below 0.1 ppt for spawning areas.It is useful to speculate whether or not fish that had retarded embryonic development and growth would survive to become adults in competition with stocks that were normal. I would think not. Also, from a sampling point of view, it is useless to look for those individuals or to make the gross but common error and infer from their absence that there was no harm done. Affected individuals would therefore be under-represented in a random sample.
Because of this problem I favor looking higher up the food chain in creatures like seals, otters, cormorants, herons, mergansers, eagles, orcas, fisherpeople, for the culprit pollutants and when one does this, they are richly but sadly rewarded.
Miller (1979) studied coho salmon exposure over 96 hours to TCDD and made 114 days of follow up observations. He found little or no bioconcentration from water below 0.1 ppt and no effect on food intake, growth or survival at 1 ppt. However, at as little as 10 ppt, there was reduced growth, survival, and food intake. Miller found that throughout his studies, fish wasted away. This wasting syndrome was characterized by reduced physical activity, reduced feeding and growth, and it often appeared long after the exposure period. Fin rot and skin lesions were also a common feature of this wasting syndrome. Argues for less than 1.0 ppt water concentration for coho with a safety factor of ten.
Kenaga and Norris (1983) estimated concentrations of TCDD in fish flesh which were associated with various designated effects. They found zero mortality at 6 ppt increasing to 50% mortality at 400 ppt with 100% mortality at 29.4 ppb. Argues for 0.6 ppt in fish flesh with a safety factor of ten.
Isensee (1978) found lethality of mosquito fish at as little as 5 ppt. Clearly great species differences exist in sensitivity. MOE, Ont. (1985) “…fish exposed to 2,3,7,8-TCDD in water react to very low concentrations (1 ng/l) and usually with an extended latency period. Embryonic and larval forms appear to be most sensitive…”. Argues for 0.1 ppt water concentrations with a safety factor of ten for other mosquito fish.
Paul M. Mehrle et al. (1987) [Toxicity and bioconcentration of 2,3,7,8-tetrachlorodibenzodioxin and 2,3,7,8-tetrachlorodibenzofuran in rainbow trout. Environmental Toxicology and Chemistry 27:47-62] found that water levels as low as 38 ppq (pq/L) had irreversible harmful effects on trout and bioconcentration increased even after it had reached 28,664 times the water levels. All levels test caused mortality, reduction in growth and behaviour changes. Clearly, the safe level is below 38 ppq, so that considerable mills are discharging harmful levels. The furan lowered growth at 0.90 ng/L(ppt) and reduced survival at 3.93 ng/L. None of those fish in the green area of Table V could therefore be declared as safe from deleterious levels for certain. Argues for 3.8 ppq water levels of TCDDEQ limit for steelhead and rainbow.
They failed to mention that the immune deficiency induced by TCDD could also lead to overall greatly reduced health of stocks, perhaps leading to greater natural mortality related to diseases and contagion. The immune impact is more general among species than considered in this document and I encourage the reader to go to the literature if they wish to pursue this more fully. It would have greater importance if the immune deficiency were transferred along with the bioconcentrating OC’s up the food chain and I have every reason to believe it does. This brings me to a good point to make a diversion to organisms higher up the food chain.
All things taken together, without looking up the food chain to see what levels are being transferred by bioconcentration, argues for conservatively establishing water levels below 5 ppq and fish flesh concentration limits for daily edibility of 0.03 ppt with a 100x safety factor considering the Class 1 carcinogenciity reclassification.
PCB’s and Organochlorines (OC’s) in Marine Mammals
Table VI. OC’s in Marine Mammals
OC Levels (ug/g) Species Location DDE DDT PCB Sea lion California 852 906 Sea lion S. California 824 112 Sea lion S. California 630 652 57 Sea lion Oregon 253 272 34 Sea lion Oregon 475 28.5 Ringed seal Bothnia 200 130 Ringed seal Bothnia 210 160 Ringed seal Bothnia 125 66 Ringed seal Bothnia 200 100 Seal Waddensee 11.3 17.6 2722 Seal Waddensee 2.4 6.5 171 Seal Waddensee 5 8.5 76 Seal Waddensee 26.6 47.3 701 Seal Waddensee 8.8 12.4 231 Belugas St. Lawrence 1.1-225 5.7-576 Mean values of selected OC’s & PCB’s in marine mammals.
Source: R. F. Addison, 1989.From the latter table, by comparison with fish data given earlier, there has been a bioaccumulation or concentration by simply going up the food chain. All of the populations in Table VI are also in decline. Their food supplies must also be in serious trouble and to me it suggests another reason for the decline of the Western Atlantic Cod stocks of Canada and the north eastern USA, pollution coupled to over-fishing.The mean for the above populations was 353 ppm for PCB’s while for fish in the Danube river, it is 0.1 – 0.3 ppm. If this river is typical of what coastal seals might get in their fish, the bioconcentration factor was 1765 times.
Pierre Beland (1988) has been monitoring the St. Lawrence Belugas which have been stranded and has analyzed their tissue for pollutants. He was richly rewarded.
He found HCB, mirex, PCB’s ranging from 517 to 576 ug/g, DDT, alpha-BHC, lindane, oxychlordane, heptachlor, aldrin, dieldrin, alpha-chlordane, gamma-chlordane, heptachlor epoxide, endrin, mercury, cadmium, lead, and polycyclic aromatic hydrocarbons at the very least. These findings support my hypothesis for the decline in the Cod stocks. These chemicals will affect overall survival and damage everything including the immune systems.
This list has much in common with what is found in human mothers’ breast milk worldwide (Jensen, Allen A., 1983). See also my review of this issue at:
http://www.geocities.com/jormabio/archive/milkcarcinogens.html
This is a profound conclusion. It means that we are through all of our regulatory efforts unable to prevent the contamination of ourselves and our children or the creatures that share our environment by the same chemicals we are assured will be diluted out of existence or decomposed to harmless substances, and most of them including all of the contaminants in Belugas, are known carcinogens. This must be a wake-up call to us all that our sophisticated and pompous and secretive government agencies are simply not doing their job.
Sweden bans fish at 5 ug/g PCB’s. By this standard, none of the Marine mammals in Table VI would be legal as food, yet the Killer whales eat them, and the Polar bears eat them and the Sharks eat them, as do fox, raven and myriad other creatures. Inuit also hunt polar bears and eat them, two trophic levels above the seals. Our own bodies have become toxic waste repositories. If the WHO standard were applied, marine mammals would have to be closed probably permanently for consumption.
It is with great sadness that I must conclude that the Atlantic Ocean is seriously polluted.
OC’s and The Bald Eagles of Ontario and Quebec
Gerald McKeating publishing in Bald Eagle Days, a symposium held in Winnipeg hosted by Johnathan Gerrard in 1983 (I was asked to give a paper but declined), provided a map of historical Bald eagle nesting areas in the Great Lakes area and a map of the shotgun pattern of the sites. In the most recent survey there were only seven nesting sites in the same area, clear evidence of a biological and ecological disaster.James Grier (1974) provided a clue as to the cause of the massive decline when he reported 94 ppm DDE, 5.2 ppm Dieldrin, 434 ppm PCB’s, and 2.5 ppm Mercury in eagles. Egg shell thinning had been linked to DDT and DDE contamination, and possibly to Dieldrin and Aldrin, and reproductive impacts have been associated with the other chemicals, but most interestingly to me, all of these same contaminants are generated by Pulp mills and found in the effluent.
The Inuit PCB’s & OC’s
It was brought to my attention by a news paper article (Prince George citizen, 1989) that Inuit mothers’ milk PCB’s were in the range 0.250 to 1.0 ppm. If this finding was for whole milk which is normally 30 times less PCB than in milk fat, the Inuit have a serious problem, and if it is in the milk fat, they are near the USA limit of 1.5 ppm PCB in milk fat (US FDA, 1972a).I was very concerned about this range because levels lower that this were associated with 50% mortality in non-human primates (Allen et al. 1980) and because I knew that Inuit ate muktuk and seal liver, foods which provided much energy but which might also carry heavy OC loads. These traditional foods might put them therefore at high risk.
Allen fed his monkeys 2.5 ppm and 5.0 ppm PCB’s as Arachlor, a form generally more toxic than the normal PCB profile in the environment, but then humans also live longer than monkeys and also have multiple other exposures to complicate things. Arctic animals surveyed in 1974 had 0.3 to 21 ppm PCB’s (Clausen et al., 1974), clearly in the top end of the range Allen experimented with and most in exceedence of the Swedish 5.0 ppm limit for fish and the USA recommended limit for PCB’s of 2 ppm maximum (US FDA, 1977a). The Arctic animals surveyed included porpoises, seals, fox and polar bears.
In humans, PCB’s have been associated with 2X increased cancer death rates amongst Yusho Victims and with impacts on the immune systems (IARC 1978, Vol. 18), increased melanoma (Bann et al. 1976, 1977), and is a known liver carcinogen when ingested (Sax, 1981).
PCB’s in Quebec mothers have been increasing recently according to Dillon (J.C. Dillon et al. 1981). The surveys he refers to suggest that exceedences of the 1 ug/kg body weight limit (proposed by USA Health Protection Branch, 31 March 1978) for human milk are common, an appalling state of affairs.
PCB’s are known to occur at higher levels in nursing infants than in their mothers (Kuwabara et al. 1979, Yakushiji et al. 1979). It is this concentration effect in infants that makes them more vulnerable. This brings me to the big question, “is there any contamination of mothers’ milk in humans by mill type pollutants, and if so what explanation can we find?”
Mothers Milk OC’s and POP’s Worldwide
I have already answered that: http://www.geocities.com/jormabio/archive/milkcarcinogens.htmlCarcinogenic and endocrine disrupting Aldrin, dieldrin, DDE, beta-HCH, HCB, PCB’s, Cadmium, Lead and Mercury are all found as contaminants of mothers milk and also are generated from the Kraft process.
Dioxin and furan levels in human fat in British Columbia are indicative of a serious regulatory failure by our government (see Table VII).
Table VII. Organochlorine Levels in British Columbia Residents
Adipose Tissue, 1976
Substance Mean (ppt) TEF
2,3,7,8-TCDD 7.5 1
2,3,4,7,8 PeCDF 18.3 0.5
1,2,3,7,8 PeCDD 11.6 0.5
HxCD Furans 21.8 0.1
1,2,3,6,7,8 HxDD 117 0.1
1,2,3,4,6,7,8 HpCDF 38.3 0.01
1,2,3,4,6,7,8 HpCDD 160 0.01
OCDD 1304 0.001
Total as 2,3,7,8-TCDD 40 1
Source: Health Protection Branch, H&W Cda 1985(29)
These toxic substances no doubt leach out of numerous pulp products and re-emerge from coffee filters, tampons and toilet tissue, food packaging, from newspapers and especially from municipal incinerators and backyard garbage fires.
Cancer Deaths in Pulp Mill Workers
One would expect that all of this toxics exposure would lead to higher cancer deaths and a specific set of cancer types in pulp and paper mill workers and that is in fact the case. Additionally, a signal of dioxin appears in the fact of elevated degenerative diseases, a dioxin finding in all species tested to date. I have pulled to gether some of the key studies done prior to my review and you may access them at:http://www.geocities.com/jormabio/archive/canc_pulp_paper.html
If they are not getting into us through our water, then through our fish and if not through our fish then through our air and if not through our air, then pulp products themselves, and what is not got through these sources, is supplemented by contaminants in our food and cosmetics and inert ingredients and all the other avenues by which what we spew forth comes home to rest like the chickens and night.
Clearly, our health standards are at fault and are perhaps based more on economic pragmatism than health based goals. For example, in Table VIII, I list fish consumtion advisories and note that there is a huge discrepancy between agencies in what is recommended.
Table VIII. Health Advisories on Fish Consumption Concentration 2,3,7,8-TCDD
Health Authority Parts Per Trillion (ppt)
FDA 25
Canada 20
Michigan 10
Minnesota 1.0
EPA 0.07
Jyrkkanen 0.03
News release from the Health Division of the Oregon Dept. of Human Resources, Dec 21, 1989.
Volumes of BKME, Tonnage of OC’s in North America
Three Kraft mills in Prince George BC generate a combined total of 108, 151, 508 million cubic meters of BKME per year and discharge this into the Fraser river, British Columbia’s most important Salmon river. This amounts to an average of 36,050,502 m3/mill/year.There are 154 Kraft mills in North America so that each year, they produce 5,551,777,359 m3/BKME. That’s a lot of BKME to discharge into the environment just so I can read my newspaper.
Assume that each mill generates 50 tonnes/day (Bonsor, 1988) of chlorinated organics in the discharge stage, then by similar computations, the 154 mills would generate 2,810,500 tonnes or in kilograms, 2,810,500 x 1000kg/tonne= 2,810,500,000 kg/yr of chlorinated organics. Recall that they also unavoidably put chlorinated organics into pulp at about an equal split. These are just estimates. I don’t have exact figures but would somebody please do the checks and get back to me. For effluent levels of dioxins and furans, see http://www.geocities.com/jormabio/archive/dioxins_mill.html.
Consider also that there are similar mills in Russia and Scandinavia and South America and the Tropics.
BKME Conclusion
If these findings are not sufficient evidence to warrant finding and implementing new and safer technologies for paper production, then we might as well just cash in our chips right now. To do so will create an enormous amount of work and investment in sustainable development.Clearly, our governments need to act by taking action, not just act as Actors. Neither the current laws, nor our pollution abatement technological infrastructure nor the present system of government, are protecting people or the environment against serious, life and species threatening pollution, and it is time for a paradigm shift.
References
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Vancouver Sun, Oct. 2. 1989. Dead whale contaminated with mercury.
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