HOW SAFE ARE YOU?

Heart Centered Holistic Healer

 Dr. Stephen Duncan, D.CH.

Jesus Christ

icon for PCBs PCBs — Industrial insulators and lubricants. Banned in the U.S. in 1976. Persist for decades in the environment. Accumulate up the food chain, to man. Cause cancer and nervous system problems.

icon for Dioxins Dioxins — Pollutants, by-products of PVC production, industrial bleaching, and incineration. Cause cancer in man. Persist for decades in the environment. Very toxic to developing endocrine (hormone) system.

icon for Furans Furans — Pollutants, by-products of plastics production, industrial bleaching and incineration. Expected to cause cancer in man. Persist for decades in the environment. Very toxic to developing endocrine (hormone) system.

icon for Metals Metals — Lead, mercury, arsenic and cadmium — Cause lowered IQ, developmental delays, behavioral disorders and cancer at doses found in the environment. For lead, most exposures are from lead paint. For mercury, most exposures are from canned tuna. For arsenic, most exposures are from arsenic (CCA) treated lumber and contaminated drinking water. For cadmium, sources of exposure include pigments and bake ware.

icon for Organochlorine insecticides Organochlorine insecticides. DDT, chlordane and other pesticides. Largely banned in the U.S. Persist for decades in the environment. Accumulate up the food chain, to man. Cause cancer and numerous reproductive effects.

icon for Organophosphate insecticide metabolites Organophosphate insecticide metabolites — Breakdown products of chlorpyrifos, malathion and others. Potent nervous system toxicants. Most common source of exposure is residues in food. Recently banned for indoor uses.

icon for Phthalates Phthalates — Plasticizers. Cause birth defects of male reproductive organs. Found in a wide range of cosmetic and personal care products. Some phthalates recently banned in Europe.

icon for Volatile and Semi-volatile organic chemicals Volatile and Semi-volatile organic chemicals. — Industrial solvents and gasoline ingredients like xylene and ethyl benzene. Toxic to nervous system, some heavily used SVOCs (benzene) cause cancer.

Findings and Recommendations

In a study led by Mount Sinai School of Medicine in New York, in collaboration with the Environmental Working Group and Commonweal, researchers at two major laboratories found an average of 91 industrial compounds, pollutants, and other chemicals in the blood and urine of nine volunteers, with a total of 167 chemicals, pollutants, and pesticides found in the group.

Like most of us, none of the nine volunteers work with chemicals on the job, do not live near an industrial facility, and all lead healthy lives. Yet, the subjects contained an average of 91 compounds – most of which did not exist 75 years ago. Scientists refer to this contamination as a person’s body burden. Of the 167 chemicals found, 76 cause cancer in humans or animals, 94 are toxic to the brain and nervous system, and 79 cause birth defects or abnormal development. The dangers of exposure to these chemicals in combination has never been studied.

Study results appear in a recently-published edition of the journal Public Health Reports (Thornton, et al. 2002) – the first publicly available, comprehensive look at the chemical burden we carry in our bodies.


TABLE 1: The chemicals we found are linked to serious health problems

Health Effect or Body System Affected

Number of chemicals found in 9 people tested that are linked to the listed health impact

Average number found in 9 people

Total found in all 9 people

Range
(lowest and highest number found in all 9 people)

cancer [1]

53

76 [2]

36 to 65

birth defects / developmental delays

55

79 [3]

37 to 68

vision

5

11 [4]

4 to 7

hormone system

58

86 [5]

40 to 71

stomach or intestines

59

84 [6]

41 to 72

kidney

54

80 [7]

37 to 67

brain, nervous system

62

94 [8]

46 to 73

reproductive system

55

77 [9]

37 to 68

lungs/breathing

55

82 [10]

38 to 67

skin

56

84 [11]

37 to 70

liver

42

69 [12]

26 to 54

cardiovascular system or blood

55

82 [13]

37 to 68

hearing

34

50 [14]

16 to 47

immune system

53

77 [15]

35 to 65

male reproductive system

47

70 [16]

28 to 60

female reproductive system

42

61 [17]

24 to 56

* Some chemicals are associated with multiple health impacts, and appear in multiple categories in this table.

Source: Environmental Working Group compilation
Footnotes | References: Health Effects

These results represent the most comprehensive assessment of chemical contamination in individuals ever performed. Even so, many chemicals were not included in the analysis that are known to contaminate virtually the entire U.S. population. Two examples are Scotchgard and the related family of perfluorinated chemicals, and a group of compounds known collectively as brominated flame retardants.

A more precise picture of human contamination with industrial chemicals, pollutants and pesticides is not possible because chemical companies are not required to tell EPA how their compounds are used or monitor where their products end up in the environment. Neither does U.S. law require chemical companies to conduct basic health and safety testing of their products either before or after they are commercialized. Eighty percent of all applications to produce a new chemical are approved by the U.S. EPA with no health and safety data. Eighty percent of these are approved in three weeks.

Only the chemical companies know whether their products are dangerous and whether they are likely to contaminate people. As a first step toward a public understanding of the extent of the problem, the chemical industry must submit to the EPA and make public on the web, all information on human exposure to commercial chemicals, any and all studies relating to potential health risks, and comprehensive information on products that contain their chemicals.


Scientists have not studied the health risks of exposures to complex chemical mixtures, such as those found in this study. For two-thirds of the chemicals found, many of which are banned, researchers have partially studied the extent to which these chemicals can harm human health. They have found that these 112 compounds can threaten nearly every organ in the body at every stage of life.

In total, the nine subjects carried:

  • 76 chemicals linked to cancer in humans or animals (average of 53),
  • 94 chemicals that are toxic to the brain and nervous system (average of 62),
  • 86 chemicals that interfere with the hormone system (average of 58),
  • 79 chemicals associated with birth defects or abnormal development (average of 55),
  • 77 chemicals toxic to the reproductive system (average of 55), and
  • 77 chemicals toxic to the immune system (average of 53).


TABLE 2: 167 compounds from seven chemical groups were found in the nine people tested

 

Number of chemicals tested for in all 9 people

Total number of chemicals found in people tested

Average number of chemicals found in 9 people tested

Range of chemical concentrations found in people tested

PCBs

73

48

33

57,290 to 455,790 pg/g in blood lipid

Dioxins and furans

17

15

14

15.7 to 36.6 pg/g TEQ in blood lipid

Organophosphate pesticide metabolites

9

7

3

4.0 to 70.4 ug/L in urine

Organochlorine pesticides and metabolites

23

10

4

615 to 3084 pg/g in blood lipid (pentachlorphenol was found in 1 person at 1.4 ug/L in urine)

Phthalates

6

6

4

97.2 to 904.8 ug/g in blood lipid  

Other semivolatile and volatile chemicals (24 classes)

77

77

31

not quantified

Metals

5

4

2

varies by metal

Total

210

167

91

 

Source: EWG compilation of blood and urine analysis from two major national laboratories.



The blood and urine from the nine volunteers were tested for 210 chemicals that can be divided into seven basic groups. Of the chemical groups tested, the most prevalent were those contained in 24 classes of semivolatile and volatile chemicals, with 78 detected. These classes include well-known industrial solvents and gasoline ingredients, such as xylene and ethyl benzene, that are used in a variety of common products like paints, glues, and fire retardants. The laboratory found 48 PCBs in the nine people tested. PCBs were banned in the United States in 1976 but are used in other countries and persist in the environment for decades. Their most common use was as an insulating fluid in electrical capacitors and transformers, vacuum pumps, and gas-transmission turbines. Lead was found in all 9 participants, and mercury was found in 8.

Health professionals are not trained to link health problems to an individual’s chemical exposure, but it is increasingly evident that background exposures to industrial chemicals and pesticides are contributing to a portion of the steady increase in some health problems in the population. A number of significant health effects potentially linked to chemical exposures are increasingly prevalent:

Cancer. Between 1992 and 1999, cancer incidence increased for many forms of the disease, including breast, thyroid, kidney, liver, abdominal cavity connective tissue, skin and some forms of leukemia. The incidence of childhood cancer increased by 26 percent between 1975 and 1999, with the sharpest rise estimated for brain and other nervous system cancers (50 percent increase) and acute lymphocytic leukemia (62 percent increase). The incidence of testicular cancer also rose between 1973 and 1999 (NCI 2002). The probability that a US resident will develop cancer at some point in his or her lifetime is 1 in 2 for men and 1 in 3 for women (ACS 2001). Just 5 to 10 percent of all cancers are linked to inherited, genetic factors (ACS 2001). For the remainder, a broad array of environmental factors plays a pivotal role.

  • We found 76 carcinogens in nine people. On average, each study participant contained 53 chemical carcinogens.

Major nervous system disorders. Several recent studies have determined that the reported incidence of autism is increasing, and is now almost 10 times higher than in the mid-1980’s (Byrd 2002, Chakrabarti and Fombonne 2001, Yang, et al. 2000). The number of children being diagnosed and treated for attention deficit disorder (ADD) and attention deficit hyperactivity disorder (ADHD) has also increased dramatically in the past decade (Robison, et al. 1999, Robison, et al. 2002, Zito, et al. 2000). The causes are largely unexplained, but environmental factors, including chemical exposures, are considered a potential cause or contributor. Environmental factors have also been increasingly linked with Parkinson’s disease (Checkoway and Nelson 1999, Engel, et al. 2001).

  • We found 94 chemicals toxic to the nervous system in nine people. On average, each study participant contained 62 nervous system toxicants.

Defects of the reproductive system. Studies show that sperm counts in certain parts of the world are decreasing (Swan, et al. 2000, Toppari, et al. 1996). Scientists have measured significant regional differences in sperm count that cannot be explained by differences in genetic factors (Swan, et al. in press). Girls may be reaching puberty earlier, based on comparing current appearance of breast development and pubic hair growth with historical data (Herman-Giddens, et al. 1997). Incidence of hypospadias, a birth defect of the penis, doubled in the United States between 1970 and 1993, and is estimated to affect one of every 125 male babies born (Paulozzi, et al. 1997). The incidence of undescended testicles (cryptorchidism) and testicular cancer also appear to be rising in certain parts of the world (Bergstrom, et al. 1996, McKiernan, et al. 1999, Toppari, et al. 1996). Testicular cancer is now the most common cancer in men age 15 to 35 [NCI 2000]. Several studies have suggested links between developmental exposure to environmental contaminants and cryptorchidism or testicular cancer (Hardell, et al. in press, Hosie, et al. 2000, Toppari, et al. 1996, Weidner, et al. 1998).

  • We found 77 chemicals linked to reproductive damage in nine people. On average the nine subjects contained 55 reproductive toxicants.

Toxic effects do not require high doses

Hundreds of studies in the peer-reviewed literature show that adverse health effects from low dose exposures are occurring in the population, caused by unavoidable contamination with PCBs, DDT, dioxin, mercury, lead, toxic air pollutants, and other chemicals. The health effects scientists have linked to chemical exposures in the general population include premature death, asthma, cancer, chronic bronchitis, permanent decrements in IQ and declines in other measures of brain function, premature birth, respiratory tract infection, heart disease, and permanent decrements in lung capacity (EPA 1996, EPA 2000, Gauderman, et al. 2002, Jacobson and Jacobson 2002, Jacobson, et al. 2002, Kopp, et al. 2000, Longnecker, et al. 2001, NAS 2000, NTP 2002, Pope, et al. 2002, Salonen, et al. 1995, Sydbom, et al. 2001).

graphical link

A growing body of literature links low dose chemical exposures in animal studies to a broad range of health effects previously unexplored in high dose studies. In low dose testing, scientists are using sophisticated techniques to measure subtle but important changes in the functioning of apparently undamaged organ systems, including alterations in immune function (such as antibody response), enzyme activity, hormone levels, cellular changes in tissues, neurobehavioral parameters, organ growth, and hormone and neurotransmitter receptor levels. Importantly, many low dose effects are detected following developmental exposure. These tests focus on the effects of chemical exposures comparable to those that occur in the general population, and far below the levels that have traditionally been considered safe based on the results of studies that feed lab animals high doses of a given compound. Using these protocols, scientists are finding that low doses of chemicals can be far more harmful than previously believed.

graphical link

Low dose studies often identify toxic effects at levels far below those identified as the “no effect” level in high dose studies. For instance, through low dose studies of bisphenol A (BPA), a plasticizer chemical commonly used in dental sealants and plastic water bottles, scientists have revealed health effects at levels 2,500 times lower than EPA’s “lowest observed effect” dose, with adverse outcomes ranging from altered male reproductive organs and aggressive behavior, to abnormal mammary gland growth, early puberty, and reduced breast feeding (Figure 1).

In the face of a powerful and growing body of literature linking low dose chemical exposures and health harms in the general population, the chemical industry continues to claim that low dose exposures to hundreds of chemicals simultaneously are safe. These claims, however, are nearly always based on a lack of scientific information on the toxicity of dose exposures, not on a definitive, scientific proof of safety.

High dose animal studies provide the foundation for federal exposure limits for contaminants in consumer products, drinking water, food, and air. Indeed, the nation’s regulatory system for chemical exposures is dependent on the notion that high dose studies will reveal all the toxic properties of a chemical being tested. We now know that this is not true. A number of factors, each of which can be as important as the exposure dose, determine a compound's toxicity:

  • Timing. The timing of a dose can often determine the toxicity of the chemical. Low dose chemical exposures during fetal development or infancy are known to produce more serious toxic effects than similar exposures during adulthood for many chemicals. Lead and mercury are the classic examples, where low dose exposures in utero and during infancy cause permanent brain and nerve damage, while the same doses cause no observable effects in adults. Few high dose studies, with the exception of those required for food use pesticides, target vulnerable periods of development. Most high dose studies include only adult animals. Low dose studies almost always involve in utero exposures.
  • Genetic vulnerability. Some people are more susceptible to environmental contaminants because of genetic factors. For example, EPA-funded research has documented a 10,000-fold variability in human respiratory response to airborne particles (including allergens and pharmaceuticals) (Hattis, et al. 2001). This variability explains, in part, why we all breathe the same air, but not all of us have asthma attacks. Laboratory animal studies, often conducted with genetically-uniform animals, cannot reveal genetically-induced adverse effects that may occur in a small but significant percentage of a highly diverse human population.
  • Mechanisms. Chemicals produce a spectrum of health effects that can both vary with dose, and affect the target organ in different ways depending on dose. For instance, some chemicals produce opposite effects at high and low doses – a phenomenon called biphasic dose response. Some produce different effects at high and low doses. Some produce adverse effects at low doses, but not at higher doses. DES, a potent synthetic estrogen, has been shown to stimulate prostate growth at 0.02, 0.2, and 2 mg/kg-day, but inhibit prostate growth at doses of 100 and 200 mg/kg-day (vom Saal, et al. 1997). Perchlorate, a component of rocket fuel that contaminates drinking water, causes changes in the size of certain parts of the brain at 0.01 – 1 mg/kg-day, but not at 30 mg/kg-day (Argus 1998). Current government testing regimes do not require tests to define different effects of chemicals across a wide range of doses.

There are other problems with the assertion that all low dose exposures are safe, or trivial, simply because they are small. The chief one being that the toxicity of mixtures is almost never studied. Current high dose studies, like those required for pesticides used on food, are conducted with purified single chemicals. In the real world, people are exposed to low dose mixtures of several hundred chemicals. Scientists do not understand the toxicity of these mixtures, and with few exceptions are not investigating them.

In the rare cases in which scientists have studied the effects of mixtures, they have found adverse health effects. In two recent studies scientists dosed laboratory animals with a mixture of 16 organochlorine pesticides, lead, and cadmium, each applied at its individual regulatory “safe” dose, and found that the animals developed impaired immune response and altered function of the thyroid, a gland that is critical for brain development (Wade, et al. 2002a, Wade, et al. 2002b).

Our Body Burden

Scientists refer to the chemical exposure documented here as an individuals “body burden” – the consequence of lifelong exposure to industrial chemicals that are used in thousands of consumer products and linger as contaminants in air, water, food, and soil. There are hundreds of chemicals in drinking water, household air, dust, treated tap water and food. They come from household products like detergent, insulation, fabric treatments, cosmetics, paints, upholstery, computers and TVs, and they accumulate in fat, blood and organs, or are passed through the body in breast milk, urine, feces, sweat, semen, hair and nails. (Easton, et al. 2002, EPA 2002d, OECD 2002, Rudel, et al. 2001, Thornton, et al. 2000, USGS 2002).

We know that:

  • U.S. chemical companies hold licenses to make 75,000 chemicals for commercial use. The federal government registers an average of 2,000 newly synthesized chemicals each year.
  • The government has tallied 5,000 chemical ingredients in cosmetics; more than 3,200 chemicals added to food; 1,010 chemicals used in 11,700 consumer products; and 500 chemicals used as active ingredients in pesticides (EPA 1997c, EPA 2002b, EPA 2002c, FDA 2002a, FDA 2002b, FDA 2002c).
  • In 1998 U.S. industries reported manufacturing 6.5 trillion pounds of 9,000 different chemicals (EPA 2001), and in 2000 major U.S. industries reported dumping 7.1 billion pounds of 650 industrial chemicals into our air and water (EPA 2002a).

At least 20 major peer-reviewed scientific journals are devoted almost entirely to studies of health effects from chemical exposures. But despite the ever-growing volume of data on the nature and consequences of exposure to industrial chemicals, scientists and doctors cannot answer the most basic questions:

What health effects can be linked to the mixtures of industrial chemicals found in the human body?

Beyond a handful of chemicals, the answer is not known. The reason: there is no legal requirement to test most chemicals for health effects at any stage of production, marketing, and use.

Under the Toxic Substances Control Act (TSCA), chemical companies can continue making chemicals and putting new compounds on the market without conducting any studies of their effects on people or the environment. Some companies conduct rudimentary screening studies prior to production, but fewer than half of all applications to the EPA for new chemical production include any toxicity data at all. The government approves 80 percent of these applications with no restrictions, usually in less than three weeks. When data are provided, they are typically cursory in nature, because the government lacks the authority to request anything more than that. Eight of 10 new chemicals win approval in less than three weeks, at an average rate of seven a day. If there are no data, the government justifies approval with results of computer models that estimate if a chemical will harm human health or the environment (EPA 1997a, GAO 1994).graphical link

For chemicals that are already on the market, the EPA can request data only when it can substantiate that the chemical is causing harm, which it generally cannot do without the toxicity data it is seeking to request. In practice, this means that studies are required only after independent scientists have accumulated a body of evidence demonstrating potential harm, a process that typically takes decades.


What mixtures of industrial chemicals are found in the bodies of the general population in the U.S.?

Not known (even this study defines only a fraction of the chemicals in the nine people tested). The reason: beyond chemicals that are added to food or used as drugs, there is no requirement for chemical manufacturers to: disclose how their chemicals are used or the routes through which people are exposed; understand the fate of their chemicals in the environment; measure concentrations of their products in the environment or in people; or develop and make public analytical methods that would allow other scientists to gather information.

Companies sometimes develop methods to test for chemicals in the blood or urine of their workers, but they do not routinely disclose the methods or results to the government or the public. The government has spearheaded most of the limited testing that has been performed for the general population in studies funded by taxpayers. The government’s studies have not kept pace with the ever-expanding array of new toxic chemicals. The country’s most comprehensive program for detecting industrial chemicals in the human body is run by a government program that reported on 27 chemicals in 2001 (CDC 2001). The chemical industry provided direct funding for none of this multi-million dollar effort, but instead paid their trade association’s press office to educate the national media on the safety of industrial chemicals in the days following the government’s report release. In their upcoming report on chemical exposures, CDC is expected to release information on 116 chemicals, or about 70 percent of the number identified in this study.

A few types of consumer products, such as cosmetics and home pesticides, must carry partial ingredient labels so consumers can make informed choices. Federal law, however, does not require the chemical industry to disclose ingredients in most household consumer products, including cleaners, paints and varnishes, and chemical coatings on clothing and furniture, or the so-called “inert” ingredients in pesticides, which are typically more than 95 percent of the retail product. The EPA has compiled a database of more than 1,000 chemicals they believe might be present in 11,700 consumer products, using data the Agency gathered from chemical encyclopedias, air sampling studies in the open scientific literature, and manufacturers. But the companies have classified the chemical recipes for 9,300 of these products as “confidential business information.”

The EPA attempts to track local exposures to chemical pollutants through two testing programs, one for tap water and another for ambient air. But testing captures only a small fraction of the chemicals a person is exposed to over the course of a day. At least 165 companies have manufactured the 167 chemicals found in the test subjects, marketing them under at least 265 trade and consumer product names. By contrast, some local and state air monitoring programs track only five chemical contaminants, most of them linked to automobile exhaust. Water suppliers test tap water for 70 contaminants, but the list excludes hundreds of chemicals known to contaminate public water supplies [e.g., (USGS 2002)].

Can an individual participate in a testing program to learn what industrial chemicals are in his or her body?

Not easily. In this study the laboratory costs alone were $4,900 per person. Scientists spent two years designing the study, gaining approval of the study plan from Mount Sinai School of Medicine’s Institutional Review Board, and recruiting subjects. People can request body burden tests through their personal physicians, but in general the methods used by available commercial labs are not sensitive, the available tests are limited, or both. The CDC lists “availability of analytical methods” as one of two major constraining factors in its national biomonitoring program (CDC 2002).

Conclusions and Recommendations

This study, combined with work from the Centers for Disease Control and Prevention, and a thorough review of the scientific literature reveals a ubiquitous and insidious pollution of the human population with hundreds of chemicals, pollutants, and pesticides. In large measure this is the result of a regulatory system that leaves the EPA with few tools to study the health effects or the extent of human exposure to the thousands of chemicals found in consumer products. The widespread use of poorly studied chemicals in the absence of any meaningful regulatory structure to control them has led to:

  • Pervasive contamination of the human population with hundreds of chemicals at low dose mixtures that have not been examined for potential health effects.
  • An industry that has no legal obligation to conduct safety tests or monitor for the presence of its chemicals in the environment or the human population – and a financial incentive not to do so.
  • A federal research establishment that is unequipped, both technically and financially, to monitor the human population for commercial chemicals or to study their health effects.
  • An ever-increasing load of chemical contamination in the human population and global environment that is comprised of poorly studied chemicals, nearly all of which have never before been encountered in all of evolutionary history.

The chemical industry tightly controls the testing and the information flow on any issue related to their products. In general, the more recently a chemical has been introduced into commerce, the less scientists understand its toxicity, and the less likely it is that scientists will know how to test for it in people and the environment. The few chemicals or chemical families that have been well-studied are those for which scientists uncovered, often accidentally, environmental catastrophes that can include widespread pollution of the environment or human population.

Chemical companies are not required to disclose methods that could be used to test for their chemicals in the environment or the human body. Typically only after a compound has been on the market for decades, and has contaminated a significant portion of the environment, do independent scientists learn how to detect and quantify it. At that point, the CDC may choose to include the chemical in its national biomonitoring program. Even then there is no guarantee that the manufacturer will provide CDC with the methodology to detect it, or that the methods will be reliable. For example, three years after 3M announced that it was removing perfluorinated chemicals in Scotchgard from the market, chiefly because 3M found that the human population is widely contaminated with the chemicals, the CDC has yet to develop a method it considers reliable that would allow it to add the chemicals to its national biomonitoring program.

This situation is unacceptable.

At a minimum, people have a right to know what chemicals are in their bodies and what harm they might cause. The sole source of this information is the chemical manufacturers themselves, who historically have resisted all efforts to make basic health information on their products available to the public, regulators and independent scientists.

Without disclosure of information on the environmental fate, human contamination, and health effects of these chemicals, regulators cannot effectively prioritize efforts to reduce the health risks from the current contaminant load in the human population.

Regardless of whether or not Congress revises the nation’s laws or policies:

  • The chemical industry must submit to EPA and make public on individual company web sites, all internal studies on the properties, environmental fate, potential human exposure pathways and exposure levels, concentrations in workers and the general population, levels in the environment, worker and community health, measured effects in wildlife, toxicity, mechanisms of action and any other information relevant to human exposures and potential health effects for all chemicals reasonably likely to be found in people, drinking water, or indoor air.

Revisions to the nation’s laws and policies governing chemical manufacture and use include the following provisions:

  • Industry must be required to prove the safety of a new chemical before it is put on the market.
  • The EPA must have the unencumbered authority to request any and all new data on a chemical that is already on the market.
  • The EPA must have the clear authority to suspend a chemical’s production and sale if the data requested are not generated, or if they show that the chemical, as used, is not safe for the most sensitive portion of the exposed population.
  • Chemicals that persist in the environment or bioaccumulate in the food chain must be banned.
  • Chemicals found in humans, in products to which children might be exposed, in drinking water, food, or indoor air, must be thoroughly tested for their health effects in low dose, womb-to-tomb, multi-generational studies focused on known target organs, that include sensitive endpoints like organ function and cognitive development. Studies to define mechanisms of action (how a chemical harms the body) must also be conducted.
  • The chemical industry must develop and make public analytical methods to detect their chemicals in the human body, and conduct biomonitoring studies to find the levels of their chemicals in the general population.
  • Chemical manufacturers must fully disclose the ingredients of their products to the public.


FOOTNOTES

[1] Chemicals listed as linked to cancer are those classified by the National Toxicology Program as "known" human carcinogens, or "reasonably anticipated" to be human carcinogens; or those classified by the Environmental Protection Agency as "known" or "probable" human carcinogens.

[2] Cancer: 3 heavy metals, 1 phthalate, 9 organochlorine pesticides, 8 furans, 7 dioxins and 48 PCBs

[3] Birth defects / developmental delays: 4 heavy metals, 2 phthalates, 7 organochlorine pesticides, 8 furans, 7 dioxins, 48 PCBs and 3 other semivolatile or volatile organic compounds

[4] Vision: 1 heavy metal, 1 phthalate, 2 organochlorine pesticides and 7 other semivolatile or volatile organic compounds

[5] Hormone system: 4 heavy metals, 5 phthalates, 3 organophosphate pesticides and metabolites, 9 organochlorine pesticides, 8 furans, 7 dioxins, 48 PCBs and 2 other semivolatile or volatile organic compounds

[6] Stomach or intestines: 3 heavy metals, 3 phthalates, 2 organophosphate pesticides and metabolites, 9 organochlorine pesticides, 8 furans, 7 dioxins, 48 PCBs and 4 other semivolatile or volatile organic compounds

[7] Kidney: 4 heavy metals, 5 phthalates, 3 organochlorine pesticides, 8 furans, 7 dioxins, 48 PCBs and 5 other semivolatile or volatile organic compounds

[8] Brain, nervous system: 4 heavy metals, 4 phthalates, 7 organophosphate pesticides and metabolites, 9 organochlorine pesticides, 8 furans, 7 dioxins, 48 PCBs and 7 other semivolatile or volatile organic compounds

[9] Reproductive system: 4 heavy metals, 2 phthalates, 8 organochlorine pesticides, 8 furans, 7 dioxins and 48 PCBs

[10] Lungs/breathing: 4 heavy metals, 3 phthalates, 2 organophosphate pesticides and metabolites, 5 organochlorine pesticides, 8 furans, 7 dioxins, 48 PCBs and 5 other semivolatile or volatile organic compounds

[11] Skin: 3 heavy metals, 5 phthalates, 2 organophosphate pesticides and metabolites, 4 organochlorine pesticides, 8 furans, 7 dioxins, 48 PCBs and 7 other semivolatile or volatile organic compounds

[12] Liver: 4 heavy metals, 6 phthalates, 3 organochlorine pesticides, 48 PCBs and 8 other semivolatile or volatile organic compounds

[13] Cardiovascular system or blood: 4 heavy metals, 2 phthalates, 2 organophosphate pesticides and metabolites, 7 organochlorine pesticides, 8 furans, 7 dioxins, 48 PCBs and 4 other semivolatile or volatile organic compounds

[14] Hearing: 1 heavy metal, 48 PCBs and 1 other semivolatile or volatile organic compound

[15] Immune system: 4 heavy metals, 1 phthalate, 6 organochlorine pesticides, 8 furans, 7 dioxins, 48 PCBs and 3 other semivolatile or volatile organic compounds

[16] Male reproductive system: 4 heavy metals, 5 phthalates, 2 organochlorine pesticides, 7 dioxins, 48 PCBs and 4 other semivolatile or volatile organic compounds

[17] Female reproductive system: 2 heavy metals, 2 phthalates, 1 organochlorine pesticide, 7 dioxins, 48 PCBs and 1 other semivolatile or volatile organic compound

 

References:  Health Effects

  1. Akhtar, N, SA Kayani, MM Ahmad and M Shahab. 1996. Insecticide-induced changes in secretory activity of the thyroid gland in rats. J Appl Toxicol 16(5): 397-400.
  2. ATSDR (Agency for Toxic Substances and Disease Registry). 1992. Toxicological profile for 2-hexanone: Health effects chapter.
  3. ATSDR (Agency for Toxic Substances and Disease Registry). 1994a. Toxicological profile for chlordane: Health effects chapter.
  4. ATSDR (Agency for Toxic Substances and Disease Registry). 1994b. Toxicological profile for chlorodibenzofurans (CDFs): Health effects chapter.
  5. ATSDR (Agency for Toxic Substances and Disease Registry). 1994c. Toxicological profile for hexachlorocyclohexanes: Health effects chapter.
  6. ATSDR (Agency for Toxic Substances and Disease Registry). 1995a. Toxicological profile for diethyl phthalate (DEP): Health effects chapter.
  7. ATSDR (Agency for Toxic Substances and Disease Registry). 1995b. Toxicological profile for mirex and chlordecone: Health effects chapter.
  8. ATSDR (Agency for Toxic Substances and Disease Registry). 1995c. Toxicological profile for xylenes: Health effects chapter.
  9. ATSDR (Agency for Toxic Substances and Disease Registry). 1997. Toxicological profile for di-n-octylphthalate (DNOP): Health effects chapter.
  10. ATSDR (Agency for Toxic Substances and Disease Registry). 1998a. Toxicological profile for chlorinated dibenzo-o-dioxins (CDDs): Health effects chapter.
  11. ATSDR (Agency for Toxic Substances and Disease Registry). 1998b. Toxicological profile for chlorpyrifos: Health effects chapter.
  12. ATSDR (Agency for Toxic Substances and Disease Registry). 1999a. Toxicological profile for cadmium: Health effects chapter. Available online at http://www.atsdr.cdc.gov/toxpro2.html#Final.
  13. ATSDR (Agency for Toxic Substances and Disease Registry). 1999b. Toxicological profile for ethylbenzene: Health effects chapter.
  14. ATSDR (Agency for Toxic Substances and Disease Registry). 1999c. Toxicological profile for lead: Health effects chapter.
  15. ATSDR (Agency for Toxic Substances and Disease Registry). 2000a. Toxicological profile for arsenic: Health effects chapter.
  16. ATSDR (Agency for Toxic Substances and Disease Registry). 2000b. Toxicological profile for polychlorinated biphenyls (PCBs): Health effects chapter.
  17. ATSDR (Agency for Toxic Substances and Disease Registry). 2001. Toxicological profile for pentachlrophenol: Health effects chapter.
  18. ATSDR (Agency for Toxic Substances and Disease Registry). 2002a. Toxicological profile for DDT, DDE, DDD: Health effects chapter.
  19. ATSDR (Agency for Toxic Substances and Disease Registry). 2002b. Toxicological profile for hexachlorobenzene: Health effects chapter.
  20. ATSDR (Agency for Toxic Substances and Disease Registry). 2002c. Toxicological profile for methoxychlor: Health effects chapter.
  21. Bernard AM, de Russis R, Normand JC, Lauwerys RR. 1989. Evaluation of the subacute nephrotoxicity of cyclohexane and other industrial solvents in the female Sprague-Dawley rat. Toxicol Lett 45:271-80.
  22. BIBRA (The British Industrial Biological Research Association). 1988. Toxicity profile for cetylpyridinium chloride (CPC).
  23. Blount BC, Silva MJ, Caudill SP, Needham LL, Pirkle JL, Sampson EJ, Lucier GW, Jackson RJ, Brock JW. 2000. Levels of seven urinary phthalate metabolites in a human reference population. Environ Health Perspect 108:979-82.
  24. Bogh IB, Christensen P, Dantzer V, Groot M, Thofner IC, Rasmussen RK, Schmidt M, Greve T. 2001. Endocrine disrupting compounds: effect of octylphenol on reproduction over three generations. Theriogenology 55:131-50.
  25. Boockfor FR, Blake CA. 1997. Chronic administration of 4-tert-octylphenol to adult male rats causes shrinkage of the testes and male accessory sex organs, disrupts spermatogenesis, and increases the incidence of sperm deformities. Biol Reprod 57:267-77.
  26. Cal EPA (California Environmental Protection Agency). 1998. Lindane (gamma hexachlorocyclohexane) toxicological summary. Department of Pesticide Regulation Medical Toxicology Branch.
  27. California Department of Pesticide Regulation. 1997. Malathion: Summary of toxicology data.
  28. Cammarota M, Bevilaqua LR, Viola H, Kerr DS, Reichmann B, Teixeira V, Bulla M, Izquierdo I, Medina JH. 2002. Participation of CaMKII in neuronal plasticity and memory formation. Cell Mol Neurobiol 22:259-67.
  29. CERHR (Center for the Evaluation of Risks to Human Reproduction). 2000a. NTP-CERHR expert panel report on butyl benzyl phthlate (BBP), NTP-CERHR-BBP-00, National Toxicology Program Center for the Evaluation of Risks to Human Reproduction.
  30. CERHR (Center for the Evaluation of Risks to Human Reproduction). 2000b. NTP-CERHR expert panel report on di (2-ethylhexyl) phthalate (DEHP), NTP-CERHR-DEHP-00, National Toxicology Program Center for the Evaluation of Risks to Human Reproduction.
  31. CERHR (Center for the Evaluation of Risks to Human Reproduction). 2000c. NTP-CERHR expert panel report on di-n-butyl phthalate (DBP), NTP-CERHR-DBP-00, National Toxicology Program Center for the Evaluation of Risks to Human Reproduction.
  32. CERHR (Center for the Evaluation of Risks to Human Reproduction). 2000d. NTP-CERHR expert panel report on di-n-octyl phthalate (DnOP), NTP-CERHR-DnOP-00, National Toxicology Program Center for the Evaluation of Risks to Human Reproduction.
  33. CIR . 2002. 84th Meeting of the CIR expert panel results.
  34. Cornu MC, Lhuguenot JC, Brady AM, Moore R, Elcombe CR. 1992. Identification of the proximate peroxisome proliferator(s) derived from di (2-ethylhexyl) adipate and species differences in response. Biochem Pharmacol 43:2129-34.
  35. CPChem (Chevron Phillips Chemical Company LP). 2000. Material Safety Data Sheet for ethylcyclohexane.
  36. Dewailly E, Ayotte P, Bruneau S, Gingras S, Belles-Isles M, Roy R. 2000. Susceptibility to infections and immune status in Inuit infants exposed to organochlorines. Environ Health Perspect 108:205-11.
  37. Duty SM, Singh NP, Silva MJ, Barr D, Brock JW, Ryan L, Herrick RF, Christiani DC, Hauser R. in press 2003. The relationship between environmental exposures to phthalates and DNA damage in human sperm using the neutral comet assay. Environ Health Perspect
  38. EPA (Environmental Protection Agency). 1994. Chemical Summary for Cyclohexane (EPA 749-F-94-011a). Office of Pollution Prevention and Toxic Substances (EPA OPPTS).
  39. EPA (Environmental Protection Agency). 2000. Malathion Reregistration Eligibility Decision: Toxicology Chapther.  
  40. EPA (Environmental Protection Agency). 2001. Malathion risk assessment: Review of malathion incident reports.
  41. EPA (Environmental Protection Agency). 2002a. Methoxychlor; Tolerance Revocations: Final Rule. Federal Register July 17, 2002, Volume 67, Number 137:46906-46909.
  42. EPA (Environmental Protection Agency). 2002b. Health Effects of PCBs.
  43. Eskenazi B, Warner M, Mocarelli P, Samuels S, Needham LL, Patterson DG, Jr., Lippman S, Vercellini P, Gerthoux PM, Brambilla P, Olive D. 2002. Serum dioxin concentrations and menstrual cycle characteristics. Am J Epidemiol 156:383-92.
  44. Field EA, Price CJ, Sleet RB, George JD, Marr MC, Myers CB, Schwetz BA, Morrissey RE. 1993. Developmental toxicity evaluation of diethyl and dimethyl phthalate in rats. Teratology 48:33-44.
  45. Gray LE, Jr., Ostby J, Furr J, Price M, Veeramachaneni DN, Parks L. 2000. Perinatal exposure to the phthalates DEHP, BBP, and DINP, but not DEP, DMP, or DOTP, alters sexual differentiation of the male rat. Toxicol Sci 58:350-65.
  46. Guo YL, Hsu PC, Hsu CC, Lambert GH. 2000. Semen quality after prenatal exposure to polychlorinated biphenyls and dibenzofurans. Lancet 356:1240-1.
  47. Hosie S, Loff S, Witt K, Niessen K, Waag KL. 2000. Is there a correlation between organochlorine compounds and undescended testes? Eur J Pediatr Surg 10:304-9.
  48. HSDB (Hazardous Substances Data Bank). 2002. Cetylpyridinium chloride. National Library of Medicine (NLM) Toxicology Data Network (TOXNET¨)
  49. IPCS. 1991. Environmental Health Criteria 124: Lindane. World Health Organization - International Programme on Chemical Safety
  50. IPCS. 1997. Environmental Health Criteria 195: Hexachlorbenzene. World Health Organization - International Programme on Chemical Safety
  51. IUCLID (International Uniform Chemical Information Database). 2001. Data set: Didodecyl 3,3-thiodipropionate. US EPA AR201-13379B. December 14, 2001
  52. Katsuda S, Yoshida M, Isagawa S, Asagawa Y, Kuroda H, Watanabe T, Ando J, Takahashi M, Maekawa A. 2000. Dose- and treatment duration-related effects of p-tert-octylphenol on female rats. Reproductive Toxicology 14:119-126.
  53. Kogevinas M. 2001. Human health effects of dioxins: cancer, reproductive and endocrine system effects. Hum Reprod Update 7:331-9.
  54. Kohn MC, Parham F, Masten SA, Portier CJ, Shelby MD, Brock JW, Needham LL. 2000. Human exposure estimates for phthalates. Environ Health Perspect 108:A440-2
  55. Kreckmann KH, Baldwin JK, Roberts LG, Staab RJ, Kelly DP, Saik JE. 2000. Inhalation developmental toxicity and reproduction studies with cyclohexane. Drug Chem Toxicol 23:555-73.
  56. Laws SC, Carey SA, Ferrell JM, Bodman GJ, Cooper RL. 2000. Estrogenic activity of octylphenol, nonylphenol, bisphenol A and methoxychlor in rats. Toxicol Sci 54:154-67.
  57. Lin GH, Hemming M. 1996. Ocular and dermal irritation studies of some quaternary ammonium compounds. Food Chem Toxicol 34:177-82.
  58. Lin GH, Voss KA, Davidson TJ. 1991. Acute inhalation toxicity of cetylpyridinium chloride. Food Chem Toxicol 29:851-4.
  59. Ljung B. 2002. EU reaches agreement to impose ban on use of toxics in cosmetic products. The Bureau of National Affairs, Inc. Volume 229:November 27, 2002.
  60. Longnecker MP, Klebanoff MA, Zhou H, Brock JW. 2001. Association between maternal serum concentration of the DDT metabolite DDE and preterm and small-for-gestational-age babies at birth. Lancet 358:110-4.
  61. Malley LA, Bamberger JR, Stadler JC, Elliott GS, Hansen JF, Chiu T, Grabowski JS, Pavkov KL. 2000. Subchronic toxicity of cyclohexane in rats and mice by inhalation exposure. Drug Chem Toxicol 23:513-37.
  62. Mocarelli P, Gerthoux PM, Ferrari E, Patterson DG, Jr., Kieszak SM, Brambilla P, Vincoli N, Signorini S, Tramacere P, Carreri V, Sampson EJ, Turner WE, Needham LL. 2000. Paternal concentrations of dioxin and sex ratio of offspring. Lancet 355:1858-63
  63. Monti D, Chetoni P, Burgalassi S, Najarro M, Saettone MF. 2002. Increased corneal hydration induced by potential ocular penetration enhancers: assessment by differential scanning calorimetry (DSC) and by desiccation. Int J Pharm 232:139-47.
  64. Murature DA, Tang SY, Steinhardt G, Dougherty RC. 1987. Phthalate esters and semen quality parameters. Biomed Environ Mass Spectrom 14:473-7.
  65. NAS (National Academy of Sciences). 2000. Toxicological Effects of Methylmercury. Washington DC, National Academy Press
  66. NTP (National Toxicology Program). 1982. TR-212 carcinogenesis bioassay of di(2-ethylhexyl)adipate (CAS No. 103-23-1) in F344 Rats and B6C3F1 mice (feed study). NTIS# PB82-185927.
  67. NTP (National Toxicology Program). 2001. Chemical Repository: 2-Ethylhexyl glycidyl ether.
  68. NTP (National Toxicology Program). 2002. 10th Report on Carcinogens.
  69. OEHHA . 1997a. Public health goal for ethylbenzene in drinking water. California Environmental Protection Agency, Office of Environmental Health Hazard Assessment - Pesticide and Environmental Toxicology Section Oakland, CA
  70. OEHHA . 1997b. Public health goal for pentachlorophenol in drinking water. California Environmental Protection Agency, Office of Environmental Health Hazard Assessment - Pesticide and Environmental Toxicology Section Oakland, CA
  71. OEHHA . 2002. Draft: Public health goal for di-(2-ethylhexyl)adipate in drinking water. California Environmental Protection Agency, Office of Environmental Health Hazard Assessment - Pesticide and Environmental Toxicology Section Oakland, CA
  72. Oehlmann J, Schulte-Oehlmann U, Tillmann M, Markert B. 2000. Effects of endocrine disruptors on prosobranch snails (Mollusca: Gastropoda) in the laboratory. Part I: Bisphenol A and octylphenol as xeno-estrogens. Ecotoxicology 9:383-397.
  73. Ozmen, G and MT Akay. 1993. The effects of malathion on some hormone levels and tissues secreting these hormones in rats. Vet Hum Toxicol 35(1): 22-4.
  74. Pellizzari ED, Hartwell TD, Harris BS, 3rd, Waddell RD, Whitaker DA, Erickson MD. 1982. Purgeable organic compounds in mother's milk. Bull Environ Contam Toxicol 28:322-8.
  75. Persky V, Turyk M, Anderson HA, Hanrahan LP, Falk C, Steenport DN, Chatterton RJ, Freels S, Consortium GL. 2001. The effects of PCB exposure and fish consumption on endogenous hormones. Environmental Health Perspectives 109:1275-1283.
  76. Raychoudhury SS, Blake CA, Millette CF. 1999. Toxic effects of octylphenol on cultured rat spermatogenic cells and Sertoli cells. Toxicol Appl Pharmacol 157:192-202.
  77. Roman BL, Peterson RE. 1998. In utero and lactational exposure of the male rat to 2,3,7,8- tetrachlorodibenzo-p-dioxin impairs prostate development. 1. Effects on gene expression. Toxicol Appl Pharmacol 150:240-53.
  78. Roman BL, Timms BG, Prins GS, Peterson RE. 1998. In utero and lactational exposure of the male rat to 2,3,7,8- tetrachlorodibenzo-p-dioxin impairs prostate development. 2. Effects on growth and cytodifferentiation. Toxicol Appl Pharmacol 150:254-70.
  79. Sinha, N, B Lal and TP Singh. 1991. Pesticides induced changes in circulating thyroid hormones in the freshwater catfish Clarias batrachus. Comp Biochem Physiol C 100(1-2): 107-10.
  80. Timms BG, Peterson RE, vom Saal FS. 2002. 2,3,7,8-tetrachlorodibenzo-p-dioxin interacts with endogenous estradiol to disrupt prostate gland morphogenesis in male rat fetuses. Toxicol Sci 67:264-74.
  81. Warner M, Eskenazi B, Mocarelli P, Gerthoux PM, Samuels S, Needham L, Patterson D, Brambilla P. 2002. Serum dioxin concentrations and breast cancer risk in the Seveso Women's Health Study. Environ Health Perspect 110:625-8.
  82. WHO (World Health Organization). 1996. Guidelines for drinking-water quality, 2nd ed. Vol. 2. Health criteria and other supportive information. Geneva, World Health Organization. pp. 523-530.
  83. Yoshida M, Katsuda S, Takenaka A, Watanabe G, Taya K, Maekawa A. 2001. Effects of neonatal exposure to a high-dose p-tert-octylphenol on the male reproductive tract in rats. Toxicol Lett 121:21-33.

 


 

 

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