Health, Hormonal, and Reproductive Effects of Endocrine-Disrupting Chemicals in the Food Chain: Dioxins, PCBs, Other Organochlorine Chemicals, etc.-  Summary of Health Effects, Incidence, Areas  Affected, and Sources :   Review

(Ed: Bernard Windham, 12164 Whitehouse Rd, Tallahassee, 32317, ph 904-878-9024)

 

Introduction:   the Rapidly Growing Problem of Endocrine Disrupting Chemicals in the Environment and Food Chain

 

        The extent of the growing crisis in contamination of the environment and food chain by endocrine disrupting chemicals is reflected by the growing list of health advisories regarding eating fish and wildlife which should serve as a warning that similar bioaccumulation and effects are occurring in people as in fish and wildlife.  For 1999 the U.S. EPA list of warnings that are in effect regarding toxic levels in fish or wildlife included over 52,000 U.S. lakes, 20% of total significant lakes, all Great Lakes, and approx. 7 % of all U.S. river miles(46).   The number of health warnings rose again for mercury, PCBs. Dioxins, and DDT/DDE.   In addition to the health advisories regarding the danger in eating fish and wildlife, there are widespread findings of hormonal and reproductive disorders/failures in wildlife caused by the toxic exposures(10,112), and this is also true in most urban and industrial coastal waters(117). 

         There were approx. 50,000 warnings regarding mercury in water bodies in at least 42 states and 680 warnings in 35 states for PCBs.      A recent study found that from their food, Americans are exposed to 22 times the U.S. EPA suggested maximum level of dioxin, says a new study by scientists at the University of Texas School of Public Health at Houston.   And nursing infants commonly get 35 to 65 times the recommended dosage  said Dr. Arnold Schecter, who directed  the study. "We have to reduce the highly toxic, persistent chemicals in the environment.     The FDA Action Level for mercury and PCBs respectively are 1ppm and 3 ppm in food, while the warning levels to limit consuption are .5 ppm and .2 ppm  respectively.  The EPA drinking water standard for PCBs is .5 micrograms per liter.  The EPA drinking water standard for dioxin is 13 parts per quintillion(billion billion) since these are extremely toxic and carcinogenic.

         Large quantities of endocrine system disrupting chemicals that have adverse effects on the hormonal and reproductive systems of animals and humans have been released into the environment since WWII and are accumulating in the food chain, animals, and humans.   These chemicals have been found to act as estrogens, anti-estrogens, androgens, anti-androgens,or to interfere with thyroid hormone, cortisol, insulin, or growth regulators.  Evidence that they are having widespread catastrophic effects on wildlife and domestic animals is growing, and serious widespread effects on humans are now also being seen.


 A recent report by the National Research Council found that 50% of all pregnancies in the U.S. are now resulting in prenatal or postnatal mortality, significant birth defects, neurological conditions, or otherwise chronically unhealthy babies(1). Approximately 250,000 U.S. children are born each year with birth defects diagnosed at or shortly after birth. Birth defects are the leading cause of infant mortality in the United States.  Congenital anomalies, sudden infant death syndrome, and premature birth combined account for more than 50% of all infant mortality.

 A UK government study that looked at 9500 landfill sites and over 8 million pregnancies concluded that pregnant women have a 1% higher risk of having a baby with a congenital defect, if they live near a landfill site(125). Another study has suggested there is a 40% higher risk of congenital chromosomal abnormalities such as Down's syndrome, for people living close to the sites(125b).  The study, published in The Lancet, reveals fresh data from a 1998 study which also showed a 33% increase in the risk of non-chromosomal anomalies, such as neural-tube defects and cleft palates in people living near landfill sites. A previous UK study, funded by the government last year had found a 7% increased risk of all types of birth defects for those living within two kilometres of hazardous sites. The major finding of a recent study “is that children living near to waste sites, whether landfills or contaminated bodies of water, are hospitalized more frequently with acute respiratory infections and asthma," compared to children living in "clean" areas. (138). 

 Living within three kilometers of a landfill that accepts hazardous waste increases the risk of malformed offspring by 33 percent according to a large 1998 study called Eurohazcon conducted by eleven European university researchers using a number of congenital abnormality registries in Europe. Sixteen public health institutes were involved in the wide-ranging study(125c). Low doses of aromatic solvents were found to have endocrine effects and negative reproductive effects.  The sum of aromatic HCs (benzene, ethylbenzene, toluene, and m,p,o-xylenes) measured in exhaled breath were found to be negatively correlated with urinary endocrine markers that have been shown to be associated with nonconceptive menstrual cycles in ovulatory women(126).

 There has been a huge increase in the incidence of degenerative neurological conditions in virtually all Western countries over the last 2 decades(137). The increase in Alzheimer’s has been over 300% while the increase in Parkinson’s and other motor neuron disease has been over 50%.   The primary cause appears to be increased exposures to toxic pollutants and endocrine disrupting chemicls(137).           

       TCDD dioxin is the most toxic of a class of organochlorine chemicals including chlorinated dibenzo-p-dioxins(CDDs),dibinzofurans(CDFs), polychlorinated biphenals(PCBs), polybromodiphenyl ethers( PBDEs), brominated dibenzo-p-dioxins(BDDs), brominated dibenzofurans(BDFs), and polychlorinated pesticides.  This group have been found to have hormonal effects that disrupt the endocrine system of wildlife and humans resulting in adverse effects on reproductive system development and hormones, fetal development, and the immune system at extremely low levels of exposure (10-12,32,91,112,113,121,129,5b). Dioxins have been found to have both estrogenic and antiestrogenic effects depending on the organ or tissue affected.

The toxic metals mercury, lead, and cadmium as well as phenols have also been found to have reproductive and endocrine system disrupting effects(10-12,32,134,5a).   The ability of metals to activate estrogen receptor-alpha (ERalpha) was measured in the human breast cancer cell line, MCF-7. Similar to estradiol, treatment of cells with the divalent metals copper, cobalt, nickel, lead, mercury, tin, and chromium or with the metal anion vanadate stimulated cell proliferation; by d 6, there was a 2- to 5-fold increase in cell number. The metals also decreased the concentration of ERalpha protein and mRNA by 40-60% and induced expression of the estrogen-regulated genes progesterone receptor and pS2 by1.6- to 4-fold. Furthermore, there was a 2- to 4-fold increase in chloramphenicol acetyltransferase activity after treatment with the metals in COS-1 cells transiently cotransfected with the wild-type receptor and an estrogen-responsive chloramphenicol acetyltransferase reporter gene. The ability of the metals to alter gene expression was blocked by an antiestrogen, suggesting that the activity of these compounds is mediated by ERalpha(139). Exposure to relatively low levels of these chemicals have been documented to have had catastrophic effects on populations of Beluga whales, alligators, turtles, mink, otters, bald eagles, osprey, cormorants, terns, herring gulls, migratory birds, chickens, lake trout, chinook and coho salmon, etc. throughout the U.S. and Canada (5-12,32,34).   Farm fed salmon and salmon from Puget Sound have recently been found to have dangerous levels of PCBs(135).


        PBDEs are rapidly increasing in the the environment and food chain(122), and given their similarity in effects to PCBs and widespread nature of exposure may soon rival PCBs in terms of common adverse effects.   PBDE exposure comes from fireproofing materials in electronics, carpets, etc.  High levels of PBDEs are being found throughout the modern world in sewage sludge(which is commonly used on food crops), in waterways, fish, eggs, milk, animals, people, and mother’s milk(122).  PDBEs have been found to cause neurological and endocrine system effects similar to PCBs, as well as some being carcinogenic(121,129).  High levels of brominated flame retardants used to make household products fire-resistant are being discovered in several Arctic species including polar bears, seals, foxes, seabirds, etc.(129).  BFRs are used in television sets, car interiors, computers and some fabrics. Dr Hans Wolkers, a toxicologist at NPI, said their concentrations in the environment were doubling every five years.     "Levels of these brominated compounds are three times higher in Canadian seals than they were 10 years ago. “On Bear Island, just to the south of Svalbard, we found dead and dying gulls with PCB levels in their brains a hundred times higher than in healthy birds.  "We've found high levels of PCBs, dioxins and BFRs in the eggs.  Survival rates and average life times of polar bears are declining rapidly in areas with high levels of contamination.   "For Arctic peoples that are eating marine mammals, it's a very serious concern. "The level of pollutants in mothers' milk in Greenland is a horrific concern there, and to the broader global community. They're ingesting highly polluted food, and producing highly polluted milk."(129) Due to the these documented effects and the rapid increase in the environment, EU lawmakers have voted a broad ban on use of some types of PBDEs(123). 

       Animals and human fetal development is dependent on hormonal levels at various phases of development and the endocrine, reproductive, neurological, and immune systems are all being impacted, often seriously or catastrophically.       These chemicals are being found to have estrogenic effects(10) and/or antiandrogenic effects(48-50) on the hormonal/endocrine systems of fish, birds, and animals- resulting in effects at very low levels on the male and female reproductive organs and systems (9-12,32,20,104,107,112).  Some of the effects are immediate and acute, but other effects are less obvious and are not recognized until years later or in the next generation.   Male animals and humans in industrial countries appear to be becoming feminized through exposure to these estrogenic and antiandrogenic chemicals.    Estrogenic chemicals cause cells to produce surplus levels of estrogen, which has been linked to breast cancer, testicular cancer, lowered sperm counts, and malformation/mutations of male sex organs, and a decreased number of successful male births(63,29,31,92,93,98,104-107,118). A combination of curcumin and isoflavinoids has been found to counteract the estrogenic effects of  chemicals (128). Parabens, substances in underarm deodorants have also been found to be estrogenic, and to be commonly found in breast cancer tissue.

A new study shows that estrogenic chemicals act together to produce observable additive effects even when all of the chemicals are at concentrations below their no-observed effects concentrations(NOECs). Traditional risk assessments of estrogenic chemicals ignore the possibility of joint actions, which leads to significant underestimations of risk.  "From a regulatory point of view, the crucial question is whether the chemicals act together. Additive combination effects matter a lot because all of these agents can interact,"(124,127).  And there are thousands of such agents.  Studies have found that the combined additive or synergistic effects of such estrogenic organochlorine chemicals such as endosulfan, dieldrin, toxaphene, and chlordane are much stronger than would be expected(63).   Similar synergistic estrogenic effects were observed when small levels of estrogenic pesticides were combined with 2 types of PCBs(84) or with mercury(84b).   When a number of estrogenic chemicals at well below the no-observed-effect concentration (NOEC) were tested together, they had a significant estrogenic effect(127).

 

Effects of Endocrine Disrupting Chemicals on Fish and Wildlife

       The widespread effects observed in wildlife found to have accumulated these chemicals have now been confirmed in experimental animal studies, and a long list of additional chemicals that have estrogenic effects have been identified.  Table 1 gives a list of 46 chemicals documented to have serious endocrine system disrupting effects- including 27 insecticides or fungicides, 8 herbicides, 3 toxic metals, and 7 industrial chemicals or by products(10).    Very low levels of these chemicals are required to produce reproductive problems, birth defects, and development problems compared to even the low levels found to produce cancer.  For example only 60 parts per billion(ppb) of DDE are required to cause antiandrogenic effects on male test animals.   Lake Apopka alligators and many other populations including people have been found to have much higher levels. DDT is still a widely used chemical throughout the developing world and is dispersed all over the world by atmospheric and oceanic transport. Low levels of vinclozolin, a widely used fungicide, have similar anti-androgenic effects(49), and even lower levels of TCDD have endocrine disrupting effects on animals.  The herbicide atrazine similarly blocks testosterone binding(87), and another group of common pesticides, pyrethrins, also have been found to have anti-androgenic effects(83,5b) and to be the likely cause of enlarged breasts in men in some populations such as one in Haiti in 1981.

 

Effects of Organochlorines and Other Endocrine-disrupters on Wildlife and Animals       Studies(5b,6,7,8,9,10,11,12,32,45,51,99) have found organochlorine chemicals to be the cause of widespread catastrophic effects on wildlife including:   

   (1) eggshell thinning, deformities and high mortality in birds and eagles of    the Great Lakes        area, West Coast, New England, Florida, etc.

   (2) abnormal thyroid function in fish and birds of the Great Lakes area.

   (3) abnormal hormone levels in birds, alligators, and mammals in the Great    Lakes area,         Florida, etc.

   (4) decreased fertility in birds, fish, shellfish, otters, and minks in the  Great Lakes area, west     coast, Florida, etc.

   (5) emasculation and feminization of male fish, birds, turtles, alligators,  otters, minks, beluga         whales, polar bears, and panthers in the Great Lakes area, Florida, west coast, Europe, Arctic.

   (6) defeminization and masculation of female fish, gastropods, turtles, birds,   and mammals in     the Great Lakes area, Florida, west coast, Europe, etc.

   (7) alteration of immune function in birds and mammals of the Great Lakes area

   (8) birth defects and high infant mortality in mammals of the Great Lakes area

   (9) behavioral changes in birds of the Great Lakes and west coast areas

   (10) abnormal sex organs and intersexed birds, turtles, alligators, sturgeon, etc. in the Great            Lakes, west coast, Florida, Mississippi and Missouri Rivers, etc.

   (11) low testosterone levels and undescended testes in alligators and panthers in Florida    

   (12) strongly significant dose related relationship to endometriosis in monkeys.  

   (13)production of vitellogin, a female protein, by male fish living near sewer outfalls.

   (14) doubled rate of testicular cancer and reproductive defects in military dogs used in         Vietnam and their offspring.

    Studies have found these chemicals to be the cause of large numbers of egg mortality, infant deformities, sexual abnormalities, and population decline among birds and fish eating animals in the Great Lakes area, Florida, Arkansas, Oregon, Mississippi River, Canada, Great Britain, etc.

(5-12,32,99,107).     One type of deformity commonly caused among bird populations and in millions of commercially raised chickens exposed to low levels of dioxin or other dioxin-like chemicals is chick-edema disease, which causes twisted beaks, crooked legs, deformed claws and feathers, and other abnormalities(9).  More than 50 horses and hundreds of birds, chickens, dogs, and cats died after a horse practice area was sprayed with oil contaminated with relatively low levels of dioxin at the Shenandoah Stables near Moscow Mills, Missouri(9). 

 

    The most extensive study of organochlorine related effects are the widespread cases of eggshell  thinning, reproductive problems, and other health effects observed in the Great Lakes area as a result of DDT, PCBs, and dioxin levels for the last 3 decades.    These effects have also been observed and studied in other more isolated cases.   David Best of the U.S. Fish & Wildlife Service has been seeing increased deformities in eagles, high mortality, and reduced hatching rates(12).  He indicates no successful reproduction in the Great Lakes area and that this area acts as a "black hole" for eagles migrating from other areas.    He found eagle reproduction falls when PCBs in the body exceed 4 parts per million(ppm) or DDE levels exceeds 1 ppm.  Much higher levels are common in the Great Lakes area, with PCBs in eggs found as high as 120 ppm.   The levels of PCBs in Great Lakes fish has also been found to be the cause of reproductive system abnormalities and population declines in fish eating animals like otters and minks(12).  PCBs have been found to cause developmental and reproductive effects on wildlife at levels similar to the average levels of PCBs found in human breast milk in industrial nations like the U.S.(20,45,116).  PCBs have been shown to turn turtles that should have been males into "females" and females into feminized males at levels as low as 10 micrograms per egg.

 

        T.M. Gross of the Univ. of Florida indicates PCBs appear to have synergistic effects with those of other estrogenic chemicals like dioxin, DDT, mercury, etc.(20)   Dioxin has been found to have effects at extremely low levels(parts per trillion), but much less historic testing has been done for low levels of dioxin due to technical difficulty and expense.  Some of the wildlife effects attributed to PCBs and DDT/DDE could have been contributed to by dioxins, though laboratory studies have confirmed each of these cause effects on animals of the types seen in wildlife at levels of the pollutants observed in wildlife.

        Production of a female protein, vitelloginin, in males is turned on by estrogen and has a feminizing effect on the male reproductive system(77).  Therefore vitellogenin production in males serves as a good marker for estrogenic chemical effects.   Extremely high levels of vitelloginin and estrogen are being found in trout and carp in England, Wales, and other locations(51).  The main sources appear to be ethynlestradiol(EE-the main estrogenic chemical in birth control pills) and nonylphenols, a breakdown chemical of alkylphenol polyethoylates which are widely used in dishwashing fluids, paints, pesticides, plastics, food wraps,etc.   Nonylphenols have been found to be endocrine disrupting chemicals and to cause proliferation of cancer cell growth(98). The main source of these in streams in the U.S. and other industrial countries appears to be sewage effluent, but they are also found in food and drinking water(78).  Lab studies on animals find reproductive systems effects at levels similar to current levels of human exposure.     In another experiment, adult trout in caged pens were exposed to ethynylestradiol, a synthetic estrogen. After two months of exposure, the fish were spawned with a healthy female. Researchers discovered that the exposed trout were half as fertile as fish kept in clean water(131).

        Some of the Phthalates (plasticizers) which are the most widespread chemicals in the environment have also been found to be estrogenic, carcinogenic, and reproductive toxins in animal studies(51,79,99,109,110,140). Some phthalate esters alter gubernacular differentiation by reducing insulin-like 3 (insl3) mRNA levels(140).  Phthalates in cosmetics and fragrances have been found to cause DNA effects on sperm(110b) and the effects on the 2nd generation are more than on the generation exposed(79).  While phthalates are found in fish in fresh or marine waters exposed to sewage(99), the most common human exposure is likely from food packaging where di-butyl phthalates(DBP) levels of 50 to 500 micrograms/kg are common(80)and DEHP is likewise common. Others include BHA(a commonly used food preservative), BBP(benzy butyl phthalate-found in construction adhesives and paper food wrapping),DEP(di-ethyl phthalate-found in nail polish, dyes, plastic food wraps),  and DDP(diphenyl phthalate).  These and other xenoestrogens  also stimulated the growth of breast cancer cells in culture, and a strong case has been developed by studies that such chemicals are a significant factor in the rapid increase in breast cancer that has been observed(47,51,86).  DBP is widespread in insect repellents, plastic plumbing pipes, and plastic food wraps.  BBP is found in adhesives and paper products used in food wrapping.  BBP is often found in levels exceeding 45 mg per kg in butter and margarine(52).  Animal studies have confirmed that low levels of these chemicals alter sex hormone activities and studies in Puerto Rico indicate they are the likely cause of premature puberty in girls there, with cases occurring as early as 2 years of age(109). For a recent study period, the average age of boys developing pubic hair in the U.S. was ˝ year before the average for a past period studied(109).    DDT exposure has also been linked to premature puberty(120).The researchers found that most of the foreign  girls from developing countries  had blood levels of DDE that were 10 times higher those in native children,  "The prevalence of precocious puberty was found to be 80‑fold higher in foreign children from developing countries than in Belgian natives,"   Fetal exposure during the first trimester of pregnancy appears to have the largest effect on fetal sex organ development.  Women tested had relatively high levels of DEP and DBP.    DEHP, BBP, DBP, DEP, and DINP have all been found to lower fetal testosterone levels in animal studies at low levels and to result in male reproductive defects (110).  A federal scientific panel of the National Toxicology Program, NIEHS, concluded that  these phthalates disrupt male reproductive development.  

Another estrogenic chemical commonly found in food is bisphenol-A, which is leaching from plastic resins coating cans and baby bottles in supermarkets.  About   50 % of cans surveyed had significant levels of BPA which has been shown to cause health problems(55a).  Laboratory experiments by geneticists at Case Western Reserve University in Ohio showed that BPA disrupts the way that chromosomes align to produce the eggs of mice, leading to aneuploidy, which is the main cause of miscarriages and Down's syndrome in humans(55b).  Higher BPA exposure, reflected in higher urinary concentrations of BPA, is consistently associated with reported heart disease in the general adult population of the USA(55c).

  Beta-sitosterol, a phytoestrogenic chemical produced by tree bark and found in waters below paper mills, has been shown to affect the endocrine and reproductive systems of fish and animals below pulp plants(60,140). It has been found to significantly alter male and female reproductive hormones. Effluents from pulp and paper mills display androgenic activity of sufficient potency to masculinize and/or sex-reverse female fish.  Since sitosterol is found in the bark, much of this effect of pulp mills might be reduced by debarking pulp trees prior to grinding them up. However other chemicals which affect fish hormones such as dioxin are also found in pulp effluent. Effluent from beef cattle concentrated animal feedlot operations from the United States also displays androgenic activity in vitro, due, in part, to the presence of a steroid used to promote growth in beef cattle (140). While some of the common phthalates of weakly estrogenic, they have also been found to have more adverse synergistic effects when combined with other chemicals found in the environment and food chain.  For example, DEHP has been found to have synergistic effects with trichloroethylene and heptachlor for prenatal loss of fetus and maternal mortality in rats(81).

 

Organochlorines and Population Dieoffs of Marine Mammals

    Catastrophic declines in mammals at the top of the marine food chain such as dolphins and seals throughout the world have been traced to buildup of these chemicals in fish and the animals at the top of the marine food chain(6,10).  Fish in the North Sea and Baltic Sea have been found to have high levels of PCBs and dioxins, and a Dutch study found that seals eating fish from these areas have significantly damaged immune systems compared to seals eating less polluted fish.  Over 20,000 harbor seals died in infectious epidemics in recent years(6).

    Native groups eating these marine mammals have also been found to have high levels of PCBs and dioxins, and to have related health problems(27,37).

 

 

Organochlorines and Endocrine-disrupting Chemicals Effects in Florida

     Florida is one of the states most at risk from organochlorine and endocrine-disrupting chemicals due to its large and growing population with much higher than average emissions and sources than most other states.  Florida has the most incineration of any state(which is the number one source of dioxins and furans), and likewise has the highest per capita use of pesticides, herbicides, and fungicides, along with a large number of paper mills with dioxin in effluent.  Widespread problems in wildlife populations in Florida related to such chemicals have already been documented.    Little is known about the effects on humans in Florida as there has been virtually no testing of meat and dairy products, dioxin levels in humans or mother's milk, or of high risk populations as in some other states and countries where data is referenced.


     Lake Apopka, Florida's 3rd largest lake, is polluted with organochlorine pesticides from a chemical spill of DDT and pesticide runoff from citrus farms and muck farms.    Studies of bass, alligators, and turtles in Apopka found population densities less than 10 % that of less polluted lakes(7,8,12,5b), with sexual infertility and sexual abnormalities of males appearing to be the main cause.   Both alligators and bass were found to have abnormally high levels of estrogen and males to have very low levels of testosterone and very small penises.   This has resulted in very low levels of successful reproduction, with sperm less males, intersexed gators with testes and ovaries, and gator eggs where 90% do not survive and the rest are sexual mutants(8,12,48,5b). Dr. Guillette of the Univ. or Florida said that "if organochlorine chemicals are detrimental to embryos of other species, they are going to be detrimental to human embryos".   Bass and other fish have also been found to be unable to reproduce and to be vanishing from other formerly highly productive Florida Lakes such as in the Ocklawaha chain of Central Florida(7,5b).  Like in Apopka, the cause of reproductive failure in the fish appears to be estrogenic effects of pesticides from runoff.  The levels causing reproductive failure in fish and animals are more than 1000 times less than the level that current EPA standards for pesticide residues in food indicate is dangerous(7,5b). 

     Similar findings have been seen in dioxin or organochlorine chemically contaminated fish and wildlife of the Great Lakes region, Mississippi River, and other areas throughout the U.S. and Canada,  and in dioxin or pesticide contaminated Florida rivers (8,9,10,12,4,99).   Animal studies have confirmed that PCBs have similar feminizing and sexual mutation effects, and that there are synergistic effects between different organochlorine congeners that produce effects at lower levels than for one toxic chemical alone(12,20,124,127).  According to the U.S. EPA, there have been over 4000 listings of health bans or restrictions on eating fish due to food chain contamination in millions of lakes and rivers throughout the U.S., with over 30 states having such bans due to organochlorine chemical pollution(23 states including Florida with bans due to dioxin, 30 states for PCBs ,& 26 states for pesticides). 

 

    In addition to seven Florida rivers and portions of St Andrew Bay and Perdido Bay that have been documented to be contaminated with dioxin, over 20,000 acres of St Joseph's bay have been found to be contaminated by dangerous levels of dioxin from 2.9 to 10.9 ppt in sediments of the bay(16).   Dioxin was also found to be bioaccumulating in fish, crabs, and shellfish.  The levels in bay sediments are similar to those in other areas studied where biomagnification occurred in adult cormorants, gulls, and mergansers to levels that caused birth defects and reproductive failure(16,19).   A study of bioaccumulation of dioxin and PCBs in a bay in Lake Huron with sediment levels similar to those in St Josephs Bay found biomagnification occurred on a logarithmic scale as you go up the trophic food chain scale.    The biomagnification at the fifth trophic level of fish eating birds was 31 times the sediment levels in TCDD-equivalence and 14.2 times for  levels.     These levels resulted in widespread birth defects and reproductive failures.  A non-viable bald eagle egg had even higher levels, 1065 ppb TCDD-Eq and 58.9 ppm s.   The source of the dioxin in St Josephs Bay is effluent from a pulp and paper mill.  Due to the widespread contamination in the bay, which was one of the most pristine and productive fish, shellfish, and wildlife areas in Florida, the Fish & Wildlife Service has recommended that dioxin emissions into the bay should be eliminated by switching to a non-chlorine process that does not produce dioxins.   They have also recommended more stringent controls on dioxin than currently exist in Florida.  However these recommendations have not been approved by regulatory agencies.

   In addition to the dioxins, other similar highly toxic and carcinogenic chlorinated organic chemicals have been found in the sediments of most bays and estuaries in Florida.      A Dept. of Environmental Protection survey found polycyclic aromatic hydrocarbons(PAHs) in 70 percent of coastal sediments sampled, PCBs in 55% of sediments sampled, and chlorinated pesticides in 28% of sediments sampled(17).  These chemicals have been identified in studies as being responsible for widespread fish cancer and fish disease by scientists who participated in a Congressional Hearing on "the fish cancer epidemic in the U.S."(44) According to Senator Breux, then chairman of the fisheries committee in summing up the conference: "What we are witnessing is a natural population that is trying to show us there is something very, very wrong with the environment."

    In addition to bioaccumulation of toxic organic chemicals in fish and shellfish, the levels of highly toxic contaminants in much of the sediments sampled have been found to be toxic to marine biota and fauna in the area with many dead zones or areas with greatly reduced diversity resulting(the number of species found in sampling was less than 5 at 17% of Gulf Coast sites).   Florida Gulf Coast estuarine sediments were found to be at levels toxic to marine organisms in 20 percent of areas sampled in 1992(22), and PAHs exceeded the EPA ERL criterion (total PAH>4 ppm)in 14 % of the sediments.    Pesticides such as dieldrin, endrin, chlordane, and DDE(ERL=2.2ppb) exceeded the EPA criteria  in 23-32 percent of sediments(21,22), and heavy metals such as mercury, chromium, nickel, lead, and cadmium exceeded the standard in 11 to 22 percent of sediments. The Effects Range Low(ERL) is the concentration of a contaminant that is above 10% of the ranked contaminant levels that resulted in toxic effects.  Along with the many dioxin congeners, PCBs , chlorinated PAHs and pesticides found in the sediments of Panama City Harbor in St Andrew Bay, elevated levels of toxic metals and sulfides were also found(19).    The sediments were found to be toxic to bottom feeding amphipods.( ERL=22.7ppb) 

    These chlorinated chemicals and toxic metals are also being found in fresh water sediments and are affecting fish and wildlife throughout Florida in drainage ponds, lakes, and other inland waters(41) and similarly in other states(114-117).         Studies found widespread contamination of drainage ponds and lakes in Tallahassee and Orlando by PAHs and toxic metals from atmospheric deposition and runoff.  In a survey of the Indian River Lagoon, PAHs were found to be up to 29.4 ppm with many sites above the ERL level and 2 sites above the AET level(22 ppm-level above which biological effects always occur)(24).    PAHs are primarily the result of incomplete combustion of coal, oil, gas, and garbage.     The Indian River survey also found phthalate esters from plasticizers and highly toxic levels of tributyltin(TBT)  to be widely distributed in the lagoon(24) and referenced studies that have also found PCBs and chlorinated pesticides in the system.    Pesticides in rivers, lakes, and coastal areas come primarily from agricultural or lawn runoff.  TBT used in antifouling paints has been found to disrupt hormones controlling sexual development in mollusks at 10 parts per trillion resulting in reproductive failures and abnormalities(112).

   Pyrogenic PAHs such as benzo(a)pyrene(ERL=.43ppm,dry weight) have been shown to be highly carcinogenic, mutagenic, and teratogenic to a wide variety of organisms (21,22,24,25,53,130), as well as estrogenic(51,112,114).  PAHs have been found in animal studies to cause DNA damage that is passed on to the new generation and birth defects(130,53).   PAHs are thought to be a major factor in the increased cancer rates found in industrial countries.   In animal studies on mammals, PAHs have been shown to cause skin cancer, leukemia, breast cancer, lung cancer, lymph system cancer, and reproductive system cancers(25).   They also cause cancers in fish and other marine organisms, along with causing high chick mortality and abnormalities in birds feeding in areas with high PAHs.   PAHs have also been found to cause eye damage, cataracts, and reproductive toxicity(53).

 

    PAHs are not very soluble and tend to concentrate in sediments, organic materials, and the plant or animal food chain.  Aquatic invertebrates, fish, and amphibians collected in areas with high PAHs in sediments show elevated levels of tumors and disease(25,114).  Lower molecular weight PAHs such as naphthalenes are more acutely toxic but less carcinogenic than the high molecular weight pyrogenic PAHs. Atmospheric emissions are responsible for at least 75% of pyrogenic PAHs in aquatic environments.   The main sources of emissions are burning of organic materials in forest fires, incinerators, power plants, and home heating equipment.  Car exhaust is a lesser but very widespread source as well.  PAHs are found in plants grown in areas with high PAH deposition rates- in such cases fruits and vegetables may have up to 100 times normal levels.

 

    Toxic metals like mercury and cadmium have high levels of emissions in Florida and have also been found to have estrogenic effects at very low levels(10,5).  Mercury appears to be responsible for feminization and reproduction problems of beluga whales and polar bears in the Arctic and panthers and alligators in Florida(12,40,129,NIEHS-29) along with other effects and population declines of fish eating predators(40).  In recent years 67% of male panther cubs born have had undescended testicles, low testosterone levels, abnormal sperm, and very high estrogen levels.    Recent tests show some males have estrogen levels twice as high as testosterone levels and some females have higher testosterone levels than estrogen levels(12).     Levels of mercury in Florida are also sufficient to have contaminated lakes and bays in Florida to levels where fish in over half the lakes and streams tested have levels of mercury dangerous to wildlife or humans eating the fish, and where birds and panthers in South Florida are dying as a result of mercury levels in the fish(5,40).  Panthers eat racoons and other fish predators.

 

Health Effects of Dioxins and Related Chemicals on Humans

    Dioxin is the most acutely toxic chemical and the most potent carcinogen ever tested according to the U.S. Center for Disease Control(5,9).    Dioxin causes cancer, birth defects, learning disabilities, endometriosis, depression and behavioral problems, lower sperm counts and other sexual abnormalities, atherosclerosis and heart disease, and damage to the immune system, endocrine system, liver, skin, and neuromuscular system (1-4,9,10,11,29,32,36,37,38,45, 92,95,96,98,106,112,132,133).  Industrial pesticide plant workers exposed to dioxin have been found to be more than 3 times as likely to die from cancer and more than 2.5 times as likely to die from ischemic heart disease as workers of similar characteristics working in a nearby gas plant(61). Reproductive and endocrine disorders (higher incidence of abortions, infertility, late gestoses, cryptorchidism, retarded male sexual development, etc.) are common in the residents of Chapaevsk (Samara Region), one of the world's most dioxin-contaminated towns(132).   They also have been found to have disruption of the male reproductive system(104).   And the risk of dying was found to be dose related- increasing directly with increased exposure to dioxins and furans. Seafood from the Baltic Sea has been found to be highly contaminated with dioxins, and those eating such seafood regularly have been found to have dioxin levels comparable to workers that have been found to have adverse health effects(104).

 

    Dioxin along with other related organochlorine chemicals are very widespread in the environment and food chain in all areas of the country and is found in the blood, semen, breast milk, and fatty tissues of humans throughout the country (4,11,26,33,38).  Infants receive the highest dose and are also the most vulnerable(11,33).  Mercury, dioxins and PCBs all disrupt the activity of thyroid hormones, which are essential for normal neurological growth and development(38,66,74,76,108,5).  Pregnant women who suffer from hypothyroidism (underactive thyroid) have a four-times greater risk for miscarriage during the second trimester than those who don’t, and women with untreated thyroid deficiency were four-times more likely to have a child with a developmental disabilities and lower I.Q. (74)   Dioxin has also been found to cause insulin resistance and hyperinsulinemia(136).

    PCBs are distributed widely in the environment and cross the placenta to cause in utero injury to the developing brain (75.5). Development of the fetus is most sensitive and prenatal exposure results in developmental delays, impaired cognitive function, hyperactivity, and attention deficit disorder(75.2,75.5,95,96,4,). PCB exposure causes hypothyroidism which is one mechanism of such effects(75.5d).

 Large numbers of people are being adversely affected by dioxins and other members of its chemical family, and very small levels of dioxin cause serious adverse health effects. Vietnam War-era defoliant Agent Orange continues to contaminate livestock and fish eaten by Vietnamese decades after it was used. A 2002 study in Bien Hoa city, about 20 miles north of Ho Chi Minh City, formerly Saigon, showed residents and food had high levels of dioxin(4d).   Dioxin is still found in the bodies and sperm of Vietnam veterans 20 years after exposure (average of 49 ppt in 1987 compared to 5 ppt for controls), and Vietnam veterans’ children have experienced much higher levels of birth defects such as spina bifida and cleft palate along with much higher levels of leukemia, prostate cancer, colon cancer, male breast cancer, ischemic heart disease, motor neuron disease, and learning disabilities than normal(5,11,105). An Australian Government study of children of Vietnam veterans found higher levels of adrenal gland cancer, acute myeloid leukemia, and non-Hodgkins lymphoma than in the general population(105).  Most Americans are exposed to unhealthy levels of dioxin through normal daily consumption of food according to a recent study(101).  According to the report, children exposed to dioxins in utero during critical periods of development appear to be the most sensitive and vulnerable to the toxic effects.  Dioxin exposure has been associated with IQ defects, increased prevalence of withdrawn/depressed behavior, adverse effects on attentional processes, an increase in hyperactive behavior in children, disrupted sexual development, birth defects and damage to the immune system(75.5,101).

 

   Furans, PCBs, DDT/DDE, and other organochlorine pesticides such as endosulfan, methoxychlor, dicofol, and lindane have also been shown to be endocrine-disrupting chemicals that have health effects and adverse reproductive impacts on wildlife similar to dioxins (4,5b,10,11,12,82,85,112).     Polyaromatic hydrocarbons(PAHs) and toxic metals like mercury, cadmium, and lead also are highly neurotoxic and strong cancer promoters- in addition to being endocrine-system disrupting chemicals(5a,10,112,113). PAHs and PCBs have both been found to be among the most toxic and widespread contaminants, with both ranked in the top 10 of toxics adversely affecting the most people by U.S. EPA/ATSDR.  PAHs are increasing in lake and reservoir sediments and streams in urban areas(41) and in many bays(114,116,117). PAHs come primarily from petroleum and combustion of fossil fuels.   PAHs have been documented to cause genetic damage, malformations, reproductive failures, and reduced growth rates in fish embryos at levels as low as 0.7 ppb(114).  PCBs have similar affects on mollusks (116).  PCBs also have been found to be strong promoters of cancer, with those having over 1 ppm in blood serum having 4.5 times greater risk of non-Hodgkin’s lymphoma, the rate of occurrence of which has increased by a factor of 2.5 since 1950(90).  It is conjectured that this is due to PCBs known suppression of the immune system. The FDA Action Level for PCBs in meat(fat) is 3 ppm.

Organochlorine pesticide residue heptachlor epoxide has been found to be significantly associated with Non-Hodgkin's Lymphoma.  Higher level of dieldrin was also associated with elevated NHL risk (OR = 2.70), as were higher levels of oxychlordane, p,p ´-DDE, and ßß-benzene hexachloride (ORs = 1.79, 1.99, and 2.47, respectively). (90b)

              PCBs, dioxins, and mercury have  been found to interfere with transport of thyroid hormone which is necessary for normal growth and development(38,66,74,108,5). Higher levels of PCBs in breast milk were found to be correlated with lower levels of thyroid hormone in infants(76,108).  A relationship has been demonstrated between decreased thyroid in infants and increased risk of neurological disorders.  Humans are accumulating PCBs since they bioaccumulate and the food chain contains PCB s.   Fish collected nationwide show  residues at a level of .53 ppm, and many marine species have levels thousands of times higher(72).  A group of killer whales living off coastal British Columbia averaged 250 ppm PCBs while the females averaged 60 ppm since the majority of PCBs in a mother has been found to be transfered to the calf or infant via lactation(72).   Inuit mothers in the Arctic have extremely high levels of PCBs and toxic metals in their milk due to a diet high in fish and wildlife(37). Researchers from the Arctic Monitoring and Assessment Programme  have documented "unacceptably high levels" of man-made environmental toxins in the Inuit population of Greenland, originating from the traditional local diet of polar bears, seals and whales, a diet which until had been considered one of the healthiest on the planet. "In certain areas of East Greenland, 100% of the population were found to have levels of contamination higher than what we call a level of concern, and 30% of all tested had problematic levels” of PCBs, mercury, lead, and cadmium.. Greenland generates no notable pollution itself, and the Inuit population are in effect suffering from toxins produced elsewhere, by the world's most industrialised nations.  Authorities have found drastic increases in the levels of conditions like diabetes and heart disease in the Inuit population, that historically has seen little of such conditions.

 

 

Organochlorine and Endocrine-disrupting Chemicals Effects on Humans

    The first generation of humans widely exposed to synthetic chlorinated organic chemicals in the womb began reaching reproductive age in the 1970s. Lab experiments and studies of human exposures have demonstrated that exposures of fetuses to endocrine-disrupting chemicals can profoundly disturb organ differentiation and development of the endocrine, immune, neurological, and reproductive systems of the fetus(4,10,11,13,20,28,29,32).   Many chemicals that have estrogenic effects that disrupt the endocrine system have been identified (see  Table 1), as well as a large group of chemicals that affect the reproductive systems of male fish and animals through antiandrogenic effects (47,48,49,50).

     Studies have found mother's pass hormone-mimicking chemicals to a fetus or child through blood before birth and through breast feeding after birth, with widespread serious consequences including size, behavior, and intellectual development(10,29,31,33,38,75.5,91).


  International data from industrial countries using thousands of men show average sperm densities have fallen over 40% along with an additional drop in sperm volume of 20% and increased sperm  abnormalities in the last 50 years (over 50% decline in overall sperm counts) (10,29,31,92,98). Researchers at the National Institute of Health found that the average decline in the U.S. has been about `1.5% with an even larger decline in Europe(93).  The declines vary geographically but the largest declines have been seen in urban areas.  A study of sperm counts at a Paris sperm bank found a large decline of 33% in sperm density over the last 20 years in a group of men followed in a carefully controlled study, with the decline averaging over 2.5 % per year and an increase in abnormal sperm of 0.7% per year(NEJM,31).  Researchers at Florida State Univ. reported similar findings(4). Since 1970 significant reductions in the proportion of boys to girls born have been documented in Denmark, Netherlands, U.S. Canada, Sweden, Germany, Norway, and Finland.  Researchers suspect that disruption of normal male fetal development by environmental pollutants is the cause of these problems and trends(93). Steroidal hormones such as estradiol, testosterone, and progesterone  that are given to the majority of beef and dairy cows also appear to be an increasing factor, with levels in meat products testing at up to 30 times normal levels of such hormones(94). Heavy use by the U.S. meat industry of such hormones led to the European Union banning imports of U.S. beef in 1988.  Such practices are banned in Europe.

  Occupational exposure to certain pesticides have been found to result in reduced sperm counts and infertility(65) and similar for wildlife exposures(5b).  There has been a more than 200% increase in male reproductive problems such as cryptorchidism(undescended testicles), hypospadias, abnormal sperm, and testicular cancer in the U.S. and England since 1969 (10,29,31,92,93,98).  In a group of London men, these problems were also accompanied by significant increases in sperm abnormalities including a twelvefold increase in the number of men producing mostly abnormal sperm in the 1980s compared to the 1970s(29).     A factor in this increase appears to be increased estrogenic chemicals in river drinking water in the London area.   During this period there has also been a significant increase in breast cancer, testicular cancer, and prostrate cancer in the U.S., and an over 400% increase in ectopic pregnancies (outside the womb) and increased endometriosis in women.     Follow up studies and laboratory animal studies have confirmed a relation of these conditions with hormone mimicking estrogenic chemicals such as DES, dioxin, PCBs, DDT, etc. which have been increasing widely distributed in the environment since the 1950s.

    A strong case has been developed that xenoestrogens in the food chain are a major factor in the increase in breast cancer in the U.S. and industrial countries(51,86,98).    16-alpha-hydroxyestrone, a metabolite of the human estrogen estradiol, has been found to be strongly linked to breast cancer.  Xenoestrogenic chemicals have been found to promote breast cancer by several mechanisms- including: promotion of the bad 16-alpha form of estrogen as opposed to the good 2-alpha form; binding to estrogen receptors and inducing proliferative signals  to cells; generation of new blood vessels that aid tumor growth; damaging DNA.  Corn oil and polyunsaturated or hydrogenated fats also appear to have such estrogenic effects, while indole-3-carbinol found in plants of the broccoli family and soy products retard cancer by favoring the 2-alpha form of estrogen(51).   A synergistic effect of low levels of estrogenic chemicals has also been documented.   Mixtures of low levels of organochlorine chemicals were found to cause a significantly greater proliferation of tumor cells than when exposed individually.    This could also explain why the distribution of toxic-waste sites in the U.S. closely parallels the sites of highest breast cancer mortality(59) and increased birth defects(125).

   Women tested in a gynecological clinic with endometriosis and antihyroidal antibodies had significantly higher levels of PCBs than controls on average(100).  Organochlorine compounds also have been documented to adversely affect the immune system, resulting in increased allergic sensitivities and diseases such as eczema(102).

    Several populations of boys in Taiwan and Michigan have been monitored whose mothers were exposed to endocrine system disrupting chemicals such as dioxin and  PCBs through contaminated rice oil and eating meat grown with contaminated feed or PCBs from Lake Michigan fish(10,11,75,75.5,88,93,96,108).   These boys have developmental, psychomotor, and cognitive disfunction, along with reproductive system deformities and problems similar to some of the animal populations.    The Michigan groups effects were found to be related in a dose-dependent manner to umbilical cord serum level.  Another group whose mothers ate 2 to 3 fish per month from Lake Michigan prior to birth were found to have lower birth weight, growth retardation, low IQS, and cognitive, motor, and behavioral deficits compared to a control group.  The group having high level of PCBs later was found to display disruptive and intractable behavior.  The group with the highest prenatal exposure to PCBs had average IQ 6 points below controls and other persistent harmful developmental effects(88,75.5,34).     Other studies on children with prenatal exposure to PCBs or DDT/DDE have found similar neurological problems and learning disabilities(36,53,75,88,93),some in populations with no known special exposure.    Studies indicate at least 5% of the babies born in the U.S. are exposed to quantities of PCBs sufficient to cause neurological effects, learning disabilities, and behavioral problems.   

 Adults who eat PCB laden fish from Lake Michigan now have high levels of  (PCBs) polychlorinated biphenyls in their blood and problems with learning and memory(34).

 The researchers' latest findings show that the heavy fish eaters who are now over age 49 have problems learning and remembering new verbal information. Fish eaters with high blood PCB levels had difficulties recalling a story told just 30 minutes earlier   According to EPA and other studies this is true for an even higher percentage due to toxic metals such as lead, mercury, and cadmium(5).   

       Another similar well documented case is the experience with DES( a synthetic estrogenic chemical used to prevent spontaneous abortions from 1948 to 1971).  Daughters whose mothers took DES have been found to suffer reproductive organ disfunction, abnormal pregnancies, lowered fertility, immune system disorders,  and depression(10).   These effects are similar to those documented for animal populations with similar exposures to endocrine-disrupting chemicals.  

   The rate of depression and other similar neurological problems has increased substantially since 1945(54).  In a given year approximately 13% of women and 6% of men suffer major depression in the 1990s(54), and over 20% of all U.S children have their learning ability adversely affected by endocrine system disrupting chemicals including toxic metals (62).  Many of the organochlorine chemicals and toxic metals have been found to adversely affect the levels of brain neurotransmitter uptake of serotonin, dopamine, acetylcholine, and norepinephrine which control the brain and body's neurologic functions.  Low levels of serotonin have been shown to result in depression, anger, anxiety, aggression, violence, insomnia, obesity, sexual deviance, and other impulse disorders(62). 

 

     EPA conducts an annual survey of chemicals building up in the adipose(fatty) tissue of humans autopsied throughout the U.S. and has found levels of dioxin and organochlorine chemicals found in scientific studies to cause serious harm to wildlife and humans(10,11,26).   The average body burden in the U.S. is 9 parts per trillion(ppt), and the average dietary background exposure level of CDDs, CDFs, and PCBs is 200 to 400 picograms TEQ/ day (3 to 6 pg TEQ/ kilogram/day) (pico=1 trillionth).   Groups suffering from Chronic Fatigue Immune Dysfunction Syndrome have been found to have significantly higher levels of organochlorine chemicals than matched control groups(57).  In one study the CFIDS group averaged 100% higher levels of DDT and hexachlorobenzene than the controls.   They were also found to have a chemical in their blood similar in structure to pesticides and which appeared to have been caused by mutation of natural body bacteria. In another study over 90% of those with chronic fatigue had high levels of organochlorines and high levels of DDE(57).  Esinophils were found to be low in those with hexacholorbenene(57).   The breasts of Quebec area women with breast cancer and other groups of women with breast cancer have been found to have much higher levels of DDE than those without estrogen responsive cancer(37,51).  There is now a strong case that estrogenic chemicals are a significant factor in the increase in hormone responsive cancers(4,51). 

    Relatively high concentrations of dioxins and furans have been documented in human milk in industrial countries such as those of Europe(33).    The average daily dose of infants through breast milk is 60 pg TEQ/kg body weight/day-  10 to 20 times that of average adult exposure levels.  In a recent study of infants with average dioxin levels in this general range, the infants were divided into a high exposure and low exposure group based on mother's blood level before birth(38).   Total thyroxine and mean thyrotropin levels were somewhat higher at birth for high exposure group infants than for the low exposure group, but were significantly higher at 11 weeks old after both groups were breast fed.    Both prenatal and post natal exposures appear to produce abnormal thyroid hormone levels and affect thyroid system function.    Thyroid system function has broad effects on developing infants. Studies have found that the timing of fetal exposures is as important to effects as the magnitude of the dose; very low maternal exposures in critical window periods of fetal development can catastrophic effects(66,74)  A new study found prenatal dioxin exposure impairs the immune system (139).  This new study adds support to the hypothesis of dioxin-related immune dysfunction generated by findings from  the National Birth Defect Registry of increases in chronic infections of the ear, upper respiratory system and urinary tract in the children of Vietnam veterans who were exposed to dioxin-contaminated Agent Orange.

 

Scientific studies on animals have found as a result of dietary intake of dioxin-like compounds- at dietary intake of 1 to 1.5 parts per trillion: altered enzyme induction response and altered lymphocytes in mice(11);  at dietary intake of 4 to 25 ppt:  chloracne in rabbits, endometriosis and decreased object learning ability in monkeys, skin tumor promotion in mice, increased reproductive disorders in fetally exposed male rats, and immune system deficiency(enhanced viral susceptibility)(11,67);  general inability of monkeys to produce viable offspring at 25-50ppt dietary intake(11,68); decreased fertility in mice at 100 ppt(69); physical birth defects in mice at 1-4 ppt(70); and lower testosterone levels in rats at 15 ppb(71)     In terms of body burden of dioxin-like compounds studies found:  altered enzyme induction, altered lymphocytes, and enhanced viral susceptibility in animals at body burdens of 7 ppt(11);    decreased human testis size and altered glucose tolerance at 14 ppt(11),  decreased monkey object learning ability at 19ppt body burden;   mortality to lake trout eggs at 65 ppt, mortality to chicken embryo at 250 ppt egg wt, and mortality to rainbow trout embryos at 400 ppt(72).     These study results and body burden information do not include the many other endocrine-disrupting or estrogenic chemicals not included in the EPA study of dioxin-like chemicals.  Thus many are currently exposed to levels of endocrine-disrupting chemicals already proven to cause serious adverse effects.


     The currently used EPA and DEP risk assessment for dioxin and dioxin-like chemicals has been found to be greatly flawed and inaccurate due to the use of 1970s fish consumption data(44.1 grams/week) and failure to take into account the high risk of children, pregnant women, and groups that consume more than average amount of fish such as Native Americans, sport fishermen's families, etc. (3,7,10,14).  The average health risk from eating fish has more than quadrupled since the 1970s and is much higher for groups eating more than the average amount of fish.  According to a state survey, Florida adults eat an average of 253 grams per week of fish and 69 grams per week of shellfish(23).    Additionally the EPA risk assessment does not include the endocrine-disrupting and reproductive system effects on humans, domestic animals, and wildlife that have been widely documented.    Similarly the EPA currently does not include any of the endocrine system mediated effects discussed in this paper or food chain source effects in air emission risk assessments used in setting air emission regulations- even though EPA scientists have pointed out that these effects that are not taken into account represent over 90% of health risk to humans(4,14,42,43). 

Sources

    The U.S. uses over 178 billion kilogram of synthetic organic chemicals per year(196 million tons), of which approx. 318 million kg is pesticides(35).  The largest source of dioxins, furans, PCBs, PAHs, mercury, and cadmium is air emissions.   Dioxins and furans are chlorinated pollutants that can form during combustion of materials containing chlorine or in several industrial activities(30).   Approx. 90% of dioxins and furans are from air emissions, with incinerators and cement kilns being the largest sources(64,30,3,11,33).  Total emissions are approx. 12,500 kg per year(64), with municipal incinerators responsible for approx. 28% of known emissions and cement kilns 25%.  Incinerators have been found to produce from 514 to 5140 ng TEQ PCDD/DF gas emissions per ton of MSW(58).  Likewise about 90 % of PCBs in the Great Lakes come from air emissions(20).   PCBs historically were primarily used in electrical equipment. 

    According to the U.S. EPA, Minnesota Pollution Control Agency, and World Health Organization, the main source of dioxins in humans are contaminated dairy and beef products, along with fish and other parts of the food chain contaminated by emissions from incinerators and other combustion of chlorine compounds (3,11,14,15,30,33,42,43).  Widespread emissions containing large amounts of dioxins, mercury, cadmium and other toxics result from the over 6000 medical waste incinerators, municipal incinerators, hazardous waste incinerators, and sewer sludge incinerators.    Significant portion of hospital waste are chlorine based plastics or compounds,  MSW incinerators are the second largest source, and 40% of the waste burned in hazardous waste incinerators is chlorine compounds that produce large amounts of dioxin emissions.

    The largest cause of dioxin emissions in incinerators is combustion of PVC plastics which are extremely widespread in building materials and hospital equipment(3,11).    Burning 1 kilogram of PVC produces approx. 50 micrograms of dioxin.    The large amounts of dioxin emissions in Europe and serious health effects have caused many European countries to phase out or reduce PVC usage in packaging and other applications.  Some dairy farms in areas around incinerators have also had to be closed due to high levels of dioxins in the milk.     In addition to dioxin emissions, combustion of PVC produces over 75 other toxic emissions including vinyl chloride, PCBs, chlorobenzene, benzene, hydrogen chloride, lead, cadmium, etc.    HCl and other emissions cause acid rain, metal corrosion, and destruction of the ozone layer.   Significant levels of dioxin is found in incinerator ash which has been found to produce dangerous levels of exposure to workman, in addition to the exposure to toxic metals in the ash.  Workers and others exposed to ash or ash piles have had a high incidence of serious neurological problems.   PVC feedstock plants also emit large amounts of dioxin with high cancer rates among workers and those living around the plant.  Additionally the PVC in buildings causes many deaths or serious injuries from building fires that emit dioxins and other toxic gases. PVCs also commonly contain other toxics such as phthalates which are known reproductive toxins(21b).

    While the majority of dioxins in the food chain including fish come from atmospheric sources, high dioxin or PCB levels are also found in fish in localized areas near industrial effluent sources such as pulp mills, where fish have been found to have dangerous levels of dioxin and reproductive abnormalities in 7 Florida rivers.     Approx. 110 grams of dioxin is released by U.S. paper mills into rivers and steams each year.     This is a small fraction of that released by incinerators according to EPA(30).  Other sources of dioxins include incinerator ash, diesel vehicles, manufacturing of chlorine-rich chemicals, wood burning, and paper making(30).

 

Government Actions to Ban or Restrict Chlorinated Chemicals

    Due to the growing and well documented serious health problems being seen in animal and human populations, many Government agencies, public health, and environmental organizations have called for phasing out or severely limiting the use of chlorinated chemicals(28,13).  The International Joint Commission on the Great Lakes, the 1992 Paris Commission for the Prevention of Marine Pollution, and many U.S. or international environmental organizations have called for phasing out chlorinated chemicals.   The Society of Environmental Toxicology and Chemistry has called for restricting or banning chlorinated chemicals that are highly toxic, persistent, and bioaccumulative.   These include dioxins, furans, PCBs, and many chlorinated pesticides.   The Canadian Government announced that Canada is moving aggressively to implement this policy.    Germany and other European countries have placed severe restrictions on use of chlorinated chemicals and plastics such as PVC,  Studies also show that use of chlorine dioxide by paper mills rather than chlorine for bleaching would greatly reduce dioxin emissions, as most European countries have done(30).    In the U.S., the American Public Health Association has called for strict regulations and phaseout or cutbacks in all non-essential chlorinated chemicals, and the U.S. EPA has recommended examining chlorines impact on health and the environment- with the possible goals of banning or restricting it use. 

    A recent study has found that Trichlorophenols(TCPs) can be biodegraded in some situations by a combination of hydrogen peroxide and a catalyst

(2,9,16,23-tetra sulfopha thalocyanine)(56).

 

                                            References

 

(1)  National Academy of Sciences, National Research Council, Committee on      Developmental       Toxicology, Scientific Frontiers in Developmental Toxicology and Risk Assessment, June 1,        2000,   313 pages. & Press Release. 

(2) U.S. EPA, Hazardous Air Pollutants: Profiles of Noncancer Toxicity from

    Inhalation Exposures, EPA/600/R-93/142, 1993.

(3) Office of Technology Assessment, "Facing America's Trash, Whats Next for      Municipal Solid      Waste?",  OTA-O-424, USGPO, 1989.

(4) (a)Birth Defect/Learning Disability Registry, New Jersey Agent Orange Commission-        Association of Birth Defect Children, Fall 1993;  & (b) J.D.Erickson et al, Journal of the American Medical Assoc., 252: 903-912, 1984 & (c)ABDC News, Vol 27, No.4, march 1998, Association of Birth Defect Children; & (d) The Journal of Occupational and Environmental Medicine, Aug 2002, www.joem.org/

(5) (a) "Health Effects of Toxic Metals: Annotated Bibliography",9-1-01 (over 150 references)             B Windham (Ed) , www.flcv.com/tm98.html

        &(b)  B. Windham, "Health Effects of Pesticides: Annotated Bibliography",  6-1-01 (over 200 medical study references).  www.flcv.com/pesticid.html

(6)  Science News, Vol 146, July 1994,  "Something's Fishy",p 8-9   &  Study by   Seal

      Rehabilitation and Research Centre and Netherlands National Institute of Health, in Science, Vol 266, Nov 18 1994, p1162; & Kuehl DW, Haebler, Organochlorine, organobromine, metal and selenium residues in bottlenose dolphins in the Gulf of Mexico;     

1995; Archives of Environmental Contamination and Toxicology, 28: 494-9.

(7) T.Gross & F.Perival(Univ. of Florida) &W.Johnson(Fla. Game & Freshwater Fish                       

Commission),  study reviewed in Science News, Vol 146, Aug 13, 1994;       &                    L.J.Guillette et al,Environmental Health Perspectives, 102(8):680-688,1994;   & Human

      and Ecological Risk Assessment, 1(2):25-36.

(8) Science News, 1-8-94, p145;  &      "Lake Apopka: Gator sexual mutations likely caused by

    organochlorine  chemicals" L.Guilette, Univ. of Florida, in Tallahassee Democrat, 8-29-94; &      (31) in (5b).

(9) "Dioxins Toll on Wildlife", National Wildlife, Aug/Sept, 1994, p4-12: & Blus LJ et al,         Eggshell thinning in the brown pelican: Implication of DDE, Bioscience, 21:1213-1215; &

       Hickey JJ, Anderson DW; Chlorinted hydrocarbons and eggshell changes in fish-eating birds         1968; Science 162: 271-273. 

 (10) Dr.T. Colborn, D.Dumanoski, JP Myers(Ed.), Our Stolen Future      Dutton Books, NY, 1996; &    Chemically Induced Alterations in Functional Development-    The Wildlife,Human Connection , Princeton Scientific Press, 1992   & T. Colburn    et al, "Developmental Effects of Endocrine-Disrupting Chemicals in Wildlife and Humans",      Environmental Health Perspectives, Vol 101, No5, Oct 1993;& T.Colburn et al, "Environmentally Induced Alterations in Development,  Environmental HealthPerspectives, Supplement 4, May 1995.

(11) U.S. EPA, Health Assessment for 2,3,7,8-Tetrachlorodibenzo-p-dioxin and Related Compounds, Volume III, External Review Draft, August 1994(2000pages); & Environmental Health Risks:  EPA's Draft Reassessment of Dioxins. GAO-02-515, April 26.

      www.gao.gov/cgi-bin/getrpt?GAO-02-515 ;   & L.S. Birnbaum, "The Mechanism of  Dioxin Toxicity", Environmental Health Perspectives, 1994, Nov: 102, Suppl 9: 157-67.

(12) "Are Environmental Hormones Emasculating Wildlife", Science News, Volume 145  1994,

      p24-27  & "Another Emasculating Pesticide Found", Science News, Vol146, 1994,p16  & Science News, 1-22-94,p56 & Science News, Vol 145, 1994,p27.

(13) International Joint Commission, Supplemental Information to the Seventh  Biennial Report,

      100 Avenue Ouellete, Windsor Ontario, 1994.

(14) Minnesota Pollution Control Agency, Supplemental Health Risk Assessment Technical Working Paper, Vol I: Dioxins/Furans, Wisconsin County Resource Recovery Facility Report, April 1988.

(15) World Health Organization, "PCDD & PCDF Emissions from Incinerators-                        

Evaluation of Human Exposure", Copenhagen, 1987.

(16) G.A. Carmody et al, U.S. Fish and Wildlife Service, Preliminary Report on  Dioxin               

Contamination in St Josepths Bay to U.S. Environmental Protection  Agency, May 27, 1994

(17) Florida Dept. of Environmental Protection, Florida Coastal Sediment  

    Contaminant Atlas,  A Summary of Coastal Sediment Quality Surveys, 1994.

    & E.R.Long et al, "Incidence of Adverse Biological Effects Within Ranges of  Chemical Concentrations in Estuarine Sediments", Envir. Management, Vol 1(3)

(18) Batelle Marine Sciences Laboratory, "Ecological Evaluation of Proposed  Dredged    Material from St Andrew Bay", Batelle/Pacific Northwest Laboratory, October 1993.

(19) P.D. Jones et al, Biomagnification of Bioassay Derived TCDD-Dioxin Equivalents",       U.S. Fish & Wildlife Service, July 1992.

(20) J.M. Bergeron et al, Environmental Health Perspectives, Sept 1994  &

     "Gender Bending PCBs", Science News, Volume 146, Oct 8, 1994, p239   &  D.E.Tillet et         al,"...PCBs..." Environ Toxicol Chem 11:1281-1288, 1992.            ;  & Science News,

    1-22-94, p56; &  Science News, Vol 145, 1994, p27;  &  Science News, Vol 146,  p206;  &     & "PCB Hazards to Fish, Wildlife, and Invertebrates", U.S. Fish & Wildlife     Service,

      Contamination Hazard Reviews Biological Report 85(1.7),  1987.

(21) U.S. EPA, Contaminated Sediments News, EPA-823-N94-003, September,1994; & (b) http://www.environmentaldefence.ca/toxicnation/resources/glossary.htm#11

(22) U.S. EPA, Environmental Monitoring and Assessment Program-Estuaries-              Louisianian Province-1992 & 1991.

(23) Fla. Agricultural Market Research Center, Per Capita Fish and Shellfish

    Consumption in Florida, Fla.Dept. of Environmental Protection, August 1994.

(24) J.G. Windsor & J.M. Surman, Toxic Substances Survey for the Indian River

    Lagoon System", Vol 2, Organic Chemicals, St Johns Water Mmgt Dist, 1993.

(25) J.M.Neff, "Polycyclic aromatic hydrocarbons", in Fundamentals of Aquatic  

    Toxicology, Hemisphere Publishing Corp., New York, 1979, p416-454;

  & R.Eizler, "Polyaromatic Hydrocarbon Hazards to Fish, Wildlife, and Invertebrates", U.S. Fish &     Wildlife Service, Contamination Hazard Reviews  Biological Report        85(1.11), May 1987.

(26) U.S. EPA, Broadscan Analysis of Human Adipose Tissue, annual report,1987 ...

    & M.J.DeVito et al, Environ Health Perspectives, 103(9): 820-831,1995.

(27) "Organochlorines lace Innuit breast milk", Science News, Vol 145, Feb 12, 1994;

       & P. Ayotte et al, Environmental Health Perspectives, Dec 1993, p618.

(28) "The Role of Chlorine and Its Future", Science News, Vol 145, June 1994, p59       & Science News,      Vol 146, Sept 10, 1994, p56-59 & Science News, 1-22-94,          p59.

(29) C.Chivers et al, "Apparent doubling of frequency of undescended testicles in England and Wales, 1962-1981",Lancet i:330-332, 1984;  &  M.B. Jackson et al, British Medical Journal, 293:1401-4,1986 +”The Epidemiology of Cryptorchidism”,   Hormone Research, Vol 30, 1988,p153-156;  &  Science News, Vol 145, Jan 22, 1994, p56-59;   & A.Giwercman et al, Environ Health Persp 101(Sup2):1993   &  Science News, 1-8-94, p 24; & Science News, 2-26-86, p264;   &  "Sperm changes linked to River Drinking Water", Science News, Vol 145, 1994, p142; &    A.Giwercman et al, “The human testis: an organ at risk”,  International Journal of      Andrology, vol 15, 1992; & A.Osterlind, “Trends in testicular cancer in Denmark”, British J of Cancer, Vol 53, 1986, p501-503; & A.R. Moss et al, “Hormonal Risk Factors in in testicular cancer”, American J of Epidemiology, Vol 124, 1986;        & M.B. Jackson et al, “The Epidemiology of  Cryptorchidism”, Hormone Research, Vol 30, 1988; & J.Toppari et al,  NIEHS, Envir. Health Perspectives, Vol 104,     Supp 4, August 1996, p741-803.

(30) "Dioxins Dominate Denver Gathering of Toxicologists", Science, Vol 266,

     Nov 18, 1994, p1162   & Science News, Vol 146, p206.

(31)  E.Carlsen et al, Brit Med Journal, 305:609-613, 1992; & Lancet,i:1311,1985.   &     J.Auger et al, "Decline in Sperm Quality Among Men in  Paris", New England Journal of Medicine, Vol 232, Feb 2, 1995;   & Science News, Vol 145, 1-22-94, p56;   & C.M.K.Nelson, Fertil Steril, 25:503-7,1974; &  J. Ginsberg et al, London's Royal Hospital School of Medicine, Lancet, 1994.  & D.Rajpert et al, Eur Urol 23:54-61, 1993;  &  C.A. Kimmel, Environ Health Perspectives, 101(Suppl 2): 137-143, 1993;  &  U.S. GAO, Reproductive and  Developmental Toxicants, Washington D.C. 1993.

(32) "Dioxins are more than carcinogens", Vol 146, Sept 17, 1994, p181,   &

     Science News, 1-11-92  & Science News, 11-27-93  & Science News, 1-8-94.

(33) WHO Environmental Health Series 34, "Levels of PCBs, PCDDs, and PCDFs in Breast Milk", World Health Organization, Copenhagen, 1989; & A.H.Smith,  "Assessment of        Infant Exposure to Dioxins in Breast Milk from Incineration Emissions", Risk Anal 7(3): 347-353,1987.

(34)  S.  Schantz et al,  Eating tainted fish curbs adult learning and memory,   Environmental Health Perspectives, June 2001; & Raloff, J. 2001. Memory problems linked to PCBs in fish. Science News 159(June 16):374; & Banned pollutant's legacy: Lower IQs. Science News 1996;150(Sept. 14):165.

(35) Environmental Health Perspectives, Aug 1993, p215.

(36) J.L. Jocobson et al, "Effects of in utero exposure to PCBs on cognitive  functioning in young children", Journal of Pediatrics, Vol 116, 1990,   p38-45  &  W.J. Rogan et al, "Neonatal effects of transplacental exposure  to PCBs or DDE", Journal of Pediatrics, Vol 109, 1986, p335-341.

(37) E. Dewailly et al, Journal of the American Cancer Institute, Feb 2, 1994;  &  Environ Health

      Perspective, 101:618-620, 1993; & Dr Jens C Hansen,  Centre for Arctic Environmental Medicine at Aarhus University, Denmark, BBC News Online, Oslo, April 1, 2003

(38) J.P. Hendricks et al, "Effects of Pre- and Postnatal Exposure to Chlorinated          Dioxins and

      Furans on Human Neonatal Thyroid Hormone Concentrations", Environmental Health       Perspectives, Vol 101, No 6, Nov 1993, p504-508.

(39) H.A. Tilson et al, "PCBs and the developing nervous system",   Neurotoxicology    and    

Teratology, Vol 12, 1990.(at U.of Fla.)

(40) "Mercury found in dead Florida Bay cormorants",Tallahassee Democrat, 1-5-95; & Sepulveda MS et al, 1999, Effects of mercury on health and first-year survival of free-ranging great eggrets from southern Florida, Archives Environ Contam   and Toxicol, 37:369-376;   & C.F.Facemire et al, “Reproductive impairment in the Florida Panther”, Health Perspect,1995; & Osowski SL, 1995, The decline of mink in Georgia, North Carolina, and S. Carolina: the Role of Contaminants,  Env Contam and Toxicol, 29:418-423; & Jagoe CH, 1998, Mercury in Alligators in the Southeastern U.S., Science of the Total Envirnonment, 213:255-262,

& Esley RM, Mercury levels in alligator meat in south Louisian, 1999, Bull Environ Contam Toxicol, 63: 598-603 & DeGuise S, Lagace A, Beland P; True hermaphoditism in St Lawrence Beluga Whales, Journal of Wildlife Diseases(Delphinapterus leucas), 1994,  30: 287-290.

(41) Van Metre PC, Mahler BJ, Furlong ET, Urban sprawl leaves its PAH signiture 2000, Environmental Science and Technology, 34: 4064-4070; & "Troubled Water: Many Question Drainage Ponds' Impact on Toxins", Wall Street Journal, 1-18-95     & "Are we poisoning our lakes?",Tallahassee  Democrat, Dec 11, 1994.

(42)M. Lorber et al, U.S. EPA Office of Research and Development, Exposure Assessment Group, "Screening estimate of indirect impacts from the Columbus, Ohio incinerator",August, 19, 1994

(43) W. Farland et al, U.S. EPA Office of Research and Development, "Screening                   Analysis for WTI Incinerator", Washington D C, March 8, 1993.

(44) Representative John Breaux, Chairman of U.S. House Committee on Fisheries,

     Committee Meeting on the "Fish Cancer Epidemic in the U.S."  1984; &

B.Windham, The fish cancer epidemic and toxics(annotated bibliography), 1993.

(45) Endometriosis Association, Milwaukee, Wisconsin,1995. (414-355-2200); & Canadian Dept. of Health and Welfare, 1985,

(46) United States  Environmental Protection  Agency,    Office of Water, Novermber 2000,

The National Listing of Fish and Wildlife Advisories: Summary of 1999 Data,                       EPA‑823‑F‑00‑20, http://www.epa.gov/ost/fish/advisories/general.html;   &

  EPA. 1999, PCBs: Update on Fish Advisories.  EPA-823-F-99-019.

(47) Science News, 7-3-93, p10   &  7-15-95, p44  & 5-12-90, p303.

(48) Science News, 1-8-94 &  7-15-95,p44.

(49) W.R. Kelce & L.E. Gray, EPA, Science News, 7-2-94,p15 & 7-15-95, p45  &

    W.R. Kelce et al, EPA, Nature, 375:581-585,June 15, 1995;  & L.E.Gray et al,

    Biol Reprod.48(suppl1): p97,1993.

(50) W.R. Kelce et al, Toxicology and Applied Pharmacology, March 1995   &

     Science News, 7-15-95, p46.

(51) S.Jobling et al, Environmental Health Perspectives, 103(6):582- , 1995 &   R.E.     

      Menzer, Casarett and Doull's Toxicology, 4th ed., McGraw-Hill, 1991; &                 Science News, 7-15-95, p47 & D.L. Davis et al, "Can Environmental Estrogens   Cause Breast Cancer?" Scientific American, October, 1995, p166-

(52) Danish Environmental Protection Agency, "Male Reproductive Health and                        

Environmental Chemicals with Estrogenic Effects", Copenhagen, Denmark, 1995.

(53) U.S. EPA, Hazardous Air Pollutant Hazard Summary Fact Sheets, In Risk        

  Information System, 1995; &  Perera F, Hemminki K, et al;  In utero DNA damage from environmental pollution is associated with somatic gene mutation in newborns.  Cancer Epidemiol Biomarkers Prev 2002 Oct;11(10 Pt 1):1134-7

(54) M.N.Weissman, Columbia Univ., Science News, 12-5-92, p391.

(55) N. Olea et al, Environmental Health Perspectives, June, 1995 &  Science News, Vol 152, Oct 18,1997; & (b) P Hall et al, Bisphenol A causes aneuploidy in mice, Current Biology, March/April 2003; & (c ) D. Melzer et al, Association of Urinary Bisphenol A Concentration with Heart Disease: Evidence from NHANES 2003/06, PLoS ONE 5(1): e8673.

(56) Science News, 5-27-95.

(57) T. Roberts t al, Newcastle Univ., ABDC News, Vol 25, No. 4, 1995; &   Dunstan RH,

        Roberts TK, Donohoe M, McGregor NR, Hope D, Taylor WG, Watkins  JA, Murdoch RN,         Butt HL.   Bioaccumulated chlorinated hydrocarbons and red/white blood cell parameters.       Biochem Mol Med 1996 Jun;58(1):77‑84.

(58) P. Dyke et al, ETSU, AEA Technology, "PCDD/PCDF Releases from Various Waste      Manangement Strategies", Warmer Bulletin 46 (UK), August 1995, p22-23.

(59) Scientific American, October 1995, p32.

(60) D.L. McLatchy et al, Toxicology & Applied Pharmacology, Oct 1995;   &   Science News, Vol 148, Nov 4, 1995, p295;   &  M.E. McMaster et al,  Ecotoxicol Environ Safety 23:103-117,1992.

(61) D. Flesch, American Journal of Epidemiology, Dec 1, 1995;  & Science News,

    Vol 148, Dec 9, 1995, p399;  & Science News, 9-4-93, p149.

(62) Science News, Sept 13, 1986, p164; & NRDC Newsline, April, 1991; and

     Science News,Vol 149, Feb 10, 1996; & H.L. Needleman,Journal of American        Medical Association, Feb 7, 1996; & R.L. Siblerud et al, Psychological Reports, 74, p67-80, 1994..

(63) D.P.Crews, Univ. Of Texas, Science News, 10-8-94,p239 & 7-2-97,p69.

(64) L.P.Brzusy et al, Environmental Science & Technology, June, 1996.

(65) P.S. Larson et al, Toxicol Appl Pharmacol, 48:29-41, 1979.

(66) L.A. Couture et al, Teratology, 42: 619-627, 1990;  &  T.A. Mably et al,               Toxicol Appl Pharmacol 114: 108-117, 1992.

(67) S.E.Rier et al, Fund Appl Toxicol 21:433-441, 1993; & T.A. Mably et al,   Toxicology and Applied Pharmacology, Vol 114, May 1992, p118-126..

(68) J.R. Allen et al, Ann NY Acadamy Sci, 320:419-425, 1979;  &

     D.S. Barsotti et al, Bull. Environ. Contam Toxicol. 21:463-469, 1979.

(69) F.J.Murray et al, Toxicol Appl Pharmacol 50:241-252, 1979.

(70) H.Weber et al, Toxicol Letters, 26:159-167,1985.

(71) R.W.Moore et al, Toxicol Appl Pharmacol 109:85-97, 1991.

(72) J.B. Grieg et al, Food Cosmet Toxicol 11:585-595, 1973; & Ross PS et al, High PCB      

concentrations in Killer Whales, Marine Pollution Bulletin 2000, 40: 504-515.

(73) C.J. Schmitt et al, National Pesticide Monitoring Program, Arch Environ                 Contam         

Toxicol, 14:225-260, 1985;  &  Leifer et al, EPA-560/83-025, 1983;     


(74) J.D. McKinney et al, Environ Health Perspect 102(3): 290-297, 1994; &

Allan W.(MD),   Journal of Medical Screening, 2000; & Assoc. for Birth Defect Children,

Birth Defect News, March 2001. 

(75) CC Hsu et al, Chemosphere, 1991; & J.L. Jacobson et al, (Lake Michigan)     Journal of       

Pediatrics, 116(1): 38-45, 1990;  &  M.S.Golub et al, (...PCBs-N.           Carolina:neurobehavioral effects), Environ Health Persp 103(S2):1995,151-

(75.2) Rice D.C. U.S. EPA, Parallels between ADHD and behavioral deficits produced   by neurotoxic exposure in monkeys.  Environ Health Perspect  June 2000, Vol    108(suppl 3)

(75.5)(a)Patandin A et al, Effects of environmental exposure to PCBs and dioxins on cognitive abitlites in Dutch children. J Pediatr 1999, 134:33-41; & (b)J.L.Jacobson, S.W.Jacobson, Intelectual Impairment in Children Exposed to PCBs in utero.  N.Eng. J.Med 1996, 335:783-89;      & (c) "Environmental exposure to polychlorinated biphenyls and quality of the home environment: effects on psychodevelopment in early childhood". Lancet Vol 358, No. 10 (2001) p1602-1607; & (d) Zoeller RT. 2001 Polychlorinated Biphenyls as Disruptors of Thyroid Hormone Action. In: PCBs: Recent Advances in Environmental Toxicology and Health Effects , L.W. Robertson and L.G. Hansen, Eds. Univ Kentucky Press, Lexington. p 265-272.

(76) D.C.Morse et al, Pediatric Research 36: 468-473, 1994;   &  J.H. Kok et al, 

Pediatr Res     39:142-145,    1996.

(77) C.E. Purdom et al, Chem Ecol, 8:275-285, 1994;  &  R.M.Sharpe et al, Lancet, 1993,341:1392-; &  Environmental Health Perspectives, 103(12): 1136-1143, 1995; & G.H.Panter et al, Environmental Science and Technology, July 1, 2000; & Estrogen effects linger in male fish, Science News, 8-5-2000, 158: 94.

(78) R.White et al, (alkylphenolic estrogenic compounds), Endocrinology, 135(1):  175-   82,1994;        &  L.B.Clark et al, Intern J Environ Anal Chem 47:167-180,1992;     & G.A. Junk et al, Environ Sci    Technol 8:1100-1106, 1974.

(79) S.Jobling et al, Environ Health Perspectives, 103(6): 582-587, 1995;  &

     D.K.Gulati et al, NTIS Technical Report/PB92-111996, Sept 1991(279pp).

(80) ATSDR, Toxicological Profile of DBP, Atlanta, Ga., 1991; & ATSDR/EPA       Priority List for 1999: Top 20 Hazardous Substances, Agency for Toxic Substances     and Disease Registry,U.S. Department of Health and Human Services,                           http://www.atsdr.cdc.gov/99list.html

(81) M.G. Narotsky et al, Fund Appl Toxicol 27:203-216, 1995.

(82) P.S.Guzelian, (chlordecone), Annu Rev Pharmacol Toxicol 22:89-113,1982.

(83) M.J.Ronis et al, Abstracts of the 13th International  Neurotoxicology  Conference, Hot Springs, Ark., 1995,p16-  &  C. Eil et al, J Steroid  Biochem 35(3-4): 409-414, 1990.

(84) A.M.Soto et al, Environmental Health Perspectives, 102:380-383, 1994; & Bemis JC, Seegal RF; 2000, PCBs and methylmercury alter intracellular calcium concentrations in rat cerebellar granule cells. Neurotoxicology, 21(6): 1123-1134.

(85) P.S.Cooke et al, Biol Repro 42(3)573-583;  &  L.E. Gray et al, Toxicol Appl Pharmacol, 96(3): 525-540;  & L.E.Gray et al, Fund Appl Toxicol,12(1):92-108.

(86) M.S.Wolff et al, J.National Cancer Inst, 85(8):648-652,1993; & H.Mussslo et al,   Cancer, 66:2124-2128,1990;  &  F. Falck et al, Arch Env Health,  47(2): 143-  146,1992.

(87) J.Kniewald et al, J Appl Toxicol 15(3): 215-218, 1995.

(88) J.L.Jacobson et al, “Intelectual Impairment in children exposed to PCBs in Utero”,     New England Journal of Medicine, V 335, Sept, 1996, p783- .

(89) L.Crpem et al, Epidemiology, July 1997 & Science News, Vol 151, 6-21-97.

(90) N. Rothman et al, National Cancer Institute, Lancet, July 26, 1997 & Science  News, Aug 9, 1997,   Vol 152,p85; & L.Hardell, Orebro Medical Center Hospital; & Penelope J.E. et al, Adipose Tissue Levels of Organochlorine Pesticides and Polychlorinated Biphenyls and Risk of Non-Hodgkin's Lymphoma,  Environmental Health Perspectives Volume 112, Number 8   June 2004

(91) F.S. vomSaal, Univ. Of Missouri, Science News, 11-11-95,p310 & 10-18-97,p255

(92) D.Swan, Calif. Dept. Of Health, Environmental Health Perspectives, Nov 14,  1997, ;   & B. Schulte,Tallahassee Democrat, Nov 24, 1997, p1A.

(93) Journal of the American Medical Assoc., 1998, Vol 279; 1018-1023 & ABDC News, March    1998;  

&  Y.L Guo et al, Pollutants can affect fertility in boys, Lancet, July 12, 2002.

(94) S. Eppstein,” The Chemical Jungle: Today’s Beef Industry”, International J Of          Health Services, 1990, 20(2): 277-280; & S. Epstein, Los Angeles Times, March      20, 1994, “ A Needless New Risk of Breast Cancer”.

(95) P.Hauser et al, “Prenatal Exposures to PCBs and Dioxins: Relation to  Learning, Attention and Behavior Problems”, Toxicology & Industrial health,1998: 34:85-101.

(96) T. Colborn et al, ‘Environmental Neruotoxic Effcts: Protocols in Functional     Teratology, Toxicology and Industrial Health, 1998, Jan, 14(1-1):9-23.

(97) http://www.tmc.tulane.edu/ECME/eehome/basics/eevshorm/:

(98) ABDC News, Assoc. Of Birth Defect Children, Jan 1999; & Japanese Ministry for the Environment, News Release, Aug 3, 2001.

(99)T.Meersman, “Sexual Abnormalities in Mississippi River Walleye”, Minnesota

    Star Tribune, 4-18-99.

(100) I. Gerhard et al, “The limits of hormone substitution in pollutant exposure  and fertility disorders”, Zentralbl Gynakol, 1992, 114, 593‑602.

(101) ABDC News, Dec 1999,Assoc. For Birth Defect Children, ABDC@birthdefects.org

(102) Reichrtova E et al, “Cord Serum Immunoglobulin E Related to Enviornmental Contamination of  Human Placentas with Oganochlorine Compounds”, Envir Health Perspec, 1999, 107(11):895-99;

(103) Elaine M. Faustman, Susan M. Silbernagel, Rafael A. Ponce. Mechanisms Underlying Children's Susceptibility to Environmental Toxicants.  Environmental Health Perspectives Volume 108, Supplement 1, March 2000

(104) Mocarelli P et al, Dioxin: endocrine disruption of the male reproductive system.   Lancet, May  2000, p 1838(mocarelli@uds.unimib.it); & Kiviranta H et al, Lancet, May 2000, p1883.

(105) B. Scott, Minister for Veterans’ Affairs, Australian Institute of Health Welfare Report, Vietnam Veterans Health Study, Dec 2000. 

(106) National Institute of Environmental Health Statistics, Jan 2001 Addendum to the IEHS Ninth Report onCarcinogens;TCDD, p358A&B;http://ehis.niehs.nih.gov/roc/ninth/rahc/tcddsticker.pdf

(107) Nagler J, et al, Environmental Health Perspectives, Jan 2001, & Science News, Vol 158, Dec 23, 2000, p404-5.

(108)Stewart P; Reihman J; Lonky E; Darvill T; Pagano J.  Prenatal PCB exposure and neonatal behavioral.  Neurotoxicol Teratol 2000 Jan‑Feb;22(1):21‑9; & Susan P. Porterfield. Thyroidal Dysfunction and Environmental Chemicals‑‑Potential Impact on Brain Development; Environmental Health Perspectives; Volume 108, Supplement 3, June 2000

(109)M.E.Herman-Giddens, Age of Puberty Declining in U.S., Science News, 5-3-97, p272; &  C.J.Bourdonyetal, Environmental Health Perspectives, Sep 2000; & Science News, 9-9-2000, p165; &  M E Herman-Giddens, Chemicals, Chemicals may be contributing to early puberty,

       Archives of Pediatrics & Adolescent Medicine, Sept 2001.  

(110) J.W. Brock, U.S. CDC, Environmental Health Perspectives , & (b)Russ Hauser et al,  Harvard University School of Public Health, Link between phthalates in cosmetics and DNA damage in sperm, Environmental Health Perspectives, 2002 ; & High Levels of Phthalates found in Cosmetics,Boston Globe, www.boston.com/dailyglobe2/289/living/Scent_of_trouble_surrounds_cosm

    etics+.shtml

(111) Matthiessen P, Gibbs PE, Critical appraisal of the evidence for tributyltin-mediated endocrine disruption in molluscs. Environmental Toxicology and Chemistry, 17: 37-43/

(112) National Research Council, Hormonally Active Agents in the Environment, National Academy Press, D.C. 2000.

(113) Royal Society,   Endocrine Disrupting Chemicals  2000,   The Royal Society, London.

(114) Carls MG, Rice SD, Hose JE; Low level exposure during incubation causes malformations, genetic damage, and mortality in larval Pacific herring, Environmental Toxicology and Chemistry, 18: 481-493: & Johnson LL, Misitano D, Hom T, Contaminant effects n ovarian development and spawning success in rock sole formPuget Sound, Washington, Transactions of the American Fisheries Socienty, 127: 375-392.

(115) San Francisco Estuary Institute, Regional Monitoring Program for Trace Substances: 1995 Annual Report, Richmond  Calif.

(116) McDowell JE, Lancaster DF, Leavitt P, Ripley B.   The effects of lipophlic organic contaminants on reproductive physiology and diesease processes in marine bivalve molluscs.  Limnology and Oceanography, 44: 903-909. 

(117) Long ER, Degraded sediment quality in U.S. estuaries: a review of magnitude and ecological implications 2000, Ecological Applications 10: 338-349

(118) Guo YL, Hsu PC, Lambert GH; Semen quality after prenatal exposure to PCBs and DBFs.

         2000, 356: 1240-1241.

(119) Buck GM, Vera JE, et al; Parental Consumption of contaminated fish from Lake Ontario and prediticted fecundability, Epidemiology 2000, 11: 388-393.

(120)   JP Bourguignon et al,   Link between precocious puberty and exposure to DDT suggested.  Journal Human Reproduction, May,2001

(121)  Kim Hooper and Thomas A. McDonald, "The PBDEs: An Emerging Environmental Challenge and Another Reason for Breast-Milk Monitoring Programs," ENVIRONMENTAL HEALTH PERSPECTIVES Vol. 108, No. 5 (May 2000), pgs. 387-392; & (b) Per Eriksson and others, "Brominated Flame Retardants: A Novel Class of Developmental Neurotoxicants in Our Environment?" ENVIRONMENTAL HEALTH PERSPECTIVES Vol. 109, No. 9 (September 2001), pgs. 903-908; & (c) Zhou, T., et al. 2001. Effects of short-term in vivo exposure topolybrominated dipher ethers on thyroid hormones and hepatic enzyme activities in weanling rats. Toxicological Sciences 61(May):76; &(d) Meerts, I.A., et al. 2000. Potent competitive interactions of some brominated flame retardants and related compounds with human transthyretin in vitro. Toxicological Sciences 56(July):95:

(122) C Schubert;  PBDEs: Burned by Flame Retardants? Our bodies are accumulating chemicals from sofas, computers, and television sets.  Science News, Oct. 13, 2001; Vol. 160, No. 15;

         Per Ola Darnerud and others, "Polybrominated Diphenyl Ethers: Occurrence, Dietary Exposure, and Toxicology," ENVIRONMENTAL HEALTH PERSPECTIVES Vol. 109 Supplement 1 (March 2001), pgs. 49-68; &  Robert C. Hale and others, "Persistent pollutants in land-applied sludges," NATURE Vol. 412 (July 12, 2001), pgs. 140-141.      

 (123) C Schubert;  PBDEs: Burned by Flame Retardants? Our bodies are accumulating chemicals from sofas, computers, and television sets.  Science News, Oct. 13, 2001; Vol. 160, No. 15

(124) A Kortenkamp et al, Additive effects of estrogenic chemicals,  Evironmental Science & Technology, Apr 15, 2002, p1751-56.

(125)  P Elliot et al,  Birth defect link to landfill sites,     British Medical Journal, Aug 2001; &

  M. Vrijheid et al, Higher risk of abnormalities for people living close to landfills, Lancet, Jan 2002,

http://news.bbc.co.uk/hi/english/health/newsid_1780000/1780272.stm ; & H. Dolke et al,

Eurohazcon Report, EU, 1998 ; http://ens.lycos.com/ens/nov98/1998L‑11‑03‑01.html    & Leachate from Municipal Landfills Has Similar Toxicity to Leachate from Hazardous Waste Landfills, Rachel’s Hazardous Waste News #90   August 15, 1988,  www.ejnet.org/rachel/rhwn090a.htm

(126) S.R. Reutman et al, Evidence of Reproductive Endocrine Effects in Women with Occupational Fuel and Solvent Exposures;  Environmental Health Perspectives Volume 110, Number 8, August 2002

 (127)  N. Rajapakse, E. Silva, and A. Kortenkamp;  Combining Xenoestrogens at Levels below Individual No-Observed-Effect Concentrations Dramatically Enhances Steroid Hormone Action;  Environmental Health Perspectives Volume 110, Number 9, September 2002

(128) S. P. Verma, B. R. Goldin, and P. S. Lin;  The Inhibition of the Estrogenic Effects of Pesticides and Environmental Chemicals by Curcumin and Isoflavonoids ; Environmental Health Perspectives Volume 106, Number 12, December 1998

(129) Lars-Otto Reiersen et al,  Rovaniemi Finland, Arctic Monitoring and Assessment Program,  The Arctic Pollution 2002 Report,  (Associated Press, Oct 1, 2002); & Scientists at the Norwegian Polar Institute (NPI) in Tromso,Norway; BBC Radio 4 programme Costing The Earth,  Thursday, 26 September, 2002 (By Alex Kirby     BBC News Online environment correspondent)

(130)    C. Somers & J. Quinn, Air pollution induces heritable DNA mutations, Proceedings of the National Academy of Sciences,  www.science.mcmaster.ca/biology/faculty/quinn/quinn.htm

(131)    Irvin Schultz et al,  Battelle Marine Sciences Laboratory,  Environmental Toxicology and Chemistry, June 2003. 

(132) Revich BA.   [Chemical substances in the Russian urban environment: hazard to human health and prospects for its prevention]      Vestn Ross Akad Med Nauk. 2002;(9):45-9

(133)   Bertazzi PA, Baccarelli A, et al, Health effects of dioxin exposure: a 20-year mortality study.Am J Epidemiol. 2001 Jun 1;153(11):1031-44.

(134) Martin MB, Reiter R, Pham T, Avellanet YR, Stoica A.   Estrogen-like activity of metals in MCF-7 breast cancer cells.   Endocrinology. 2003 Jun;144(6):2425-36.

(135)       http://seattlepi.nwsource.com/local/156714_warning15.html

(136) Morris Cranmer et al,  Exposure to 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) Is Associated with Hyperinsulinemia and Insulin Resistance;  Toxicological Sciences 56, 431-436 (2000)

(137) Pritchard C. et al, Pollutants appear to be the cause of the huge rise in degenerative neurological conditions. Public Health, Aug 2004.

(138) D.O. Carpenter et al, Infection risk in children living near landfills, annual meeting of the European Respiratory Society, Sept 2006

(139) Hogaboam, J, A Moore and BP Lawrence. 2008. The aryl hydrocarbon receptor affects distinct tissue compartments during ontogeny of the immune system. Toxicological Sciences 102(1):160-170.

http://www.environmentalhealthnews.org/ehs/newscience/2007-aryl-hydrocarbon-receptor-during-ontogeny-of-the-immune-system-hogaboam-et-al/

(140) Adverse effects of environmental antiandrogens and androgens on reproductive development in mammals. Gray LE, Guillette L, et al; Int J Androl. 2006 Feb;29(1):96-108;   

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                                                             Table 1

                                                     Persistent Organohalogens

 Dioxins and furans         PBBs           PCBs          Hexachlorobenzene       Octachlorostyrene   Pentachlorophenol

 

                             

                  Pesticides

2,4,5‑T     2,4‑D     alachlor    aldicarb    d‑trans    allethrin    amitrole    atrazine     benomyl

   beta‑HCH    carbaryl     chlordane        chlozolinate            ‑cyhalothrin                  cis‑nonachlor         cypermethrin           DBCP          DDT             DDE/DDT metabolites

 dicofol      dieldrin      endosulfan       esfenvalerate      ethylparathion     fenvalerate                h‑epoxide   heptachlor  iprodione      kelthane        kepone      ketoconazole       lindane          linurone      malathion         mancozeb         maneb        methomyl       methoxychlor     metiram metribuzin        mirex         nitrofen        oxychlordane      permethrin     procymidone  sumithrin

synthetic  pyrethroids     toxaphene      trans‑nonachlor   tributyltin oxide     trifluralin

vinclozolin           zineb                        ziram

 

                                Phthalates

 

 Di‑ethylhexyl phthalate (DEHP)      Butyl benzyl phthalate (BBP)    Di‑n‑butyl phthalate (DBP) Di-n-pentyl phthalate (DPP)      Di‑hexyl phthalate (DHP)         Di‑propyl phthalate (DprP)

 Dicyclohexyl phthalate (DCHP)       Diethyl phthalate (DEP)

 

 

                            Other Compounds

 

       Penta‑ to           Nonyl‑Phenols              Bisphenol A              Bisphenol F

       Styrene dimers and trimers      Benzo(a)pyrene       ethane dimethane sulphonate

      tris‑4‑(chlorophenyl)methane          tris‑4‑(chlorophenyl)methanol

 

 

                              Heavy Metals

 

     Mercury        Lead           Cadmium

                                

   Pollutants shown to bind to hormone receptors (or to interfere

  with receptor binding) without further confirmation of endocrine   disrupting effects

 

                 2,4‑dichlorophenol               Cyanazine              Diethylhexyl adipate

                  Benzophenone                  N‑butyl benzene           4‑nitrotoluene

 

 

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