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Environmental Toxicity
The 20th century, with its promise of "better living through chemistry" has also brought a host of chemical toxin-related illnesses. Recent articles in the medical literature have shown that the rate of cancers not associated with smoking is higher for those born after 1940 than before, and that this increase of caner is due to environmental factors not related to smoking. We are also experiencing new medical diagnoses of sick building syndrome and multiple chemical sensitivity (MCS), both of which are related to overexposure to environmental contaminants.
The environmental toxins which cause the most problems are pesticides, solvents and heavy metals. The primary damage caused by the solvents and major pesticide classes is to disrupt neurological function. In addition to being neurotoxic, these compounds are profoundly immunotoxic and are often toxic to the endocrine system as well. The adverse health effects are not limited to those systems only, as these compounds can also cause a variety of dermatological, gastrointestinal, genitourinary, respiratory, musculoskeletal, and cardiological problems. Heavy metals poison a diverse range of enzyme function, affecting virtually every system of the body. The greatest exposure to heavy metals is from dental amalgam fillings and other metal dental appliances. Smoking contributes a considerable amount of cadmium into the body as well.
Our environment is currently flooded with chemicals that contaminate our air, water, food and ourselves. Since 1976, the Environmental Protection agency (EPA) has been engaged in the National Human Adipose Tissue Survey (NHATS). In this study, adipose samples are taken from cadavers and elective surgeries from all regions of the country and the levels of toxins are measured. In 1982, they expanded beyond their original list to look for the presence of 54 different environmental chemical toxins. Their results are a cause for great concern. Five of the chemicals--OCDD (a dioxin), styrene, 1,4-dichlorobenzene, xylene, and ethylphenol--were found in 100% of all samples. Another nine chemicals--benzene, toluene, chlorobenzene, ethylbenzene, DDE, three dioxins and one furan--were found in 91-98% of all samples. In addition, polychlorinated biphenols (PCBs) were found in 83% of all samples and beta-BHC in 87%. A total of 20 toxic compounds were found in 76% or more of all samples! These ongoing assessments have shown quite clearly that it is not a question of if we are carrying a burden of toxic xenobiotic compounds, but one of how much and how do they affect our health.
Additional studies have shown the same alarming facts. A CDC study of 5,994 persons aged 12-74 found that 99.5% had p,p-DDE at levels in the range 1-379 ppb. A study of adipose levels of chemicals in persons from Texas showed the presence of p,p-DDE, dieldrin, oxychlordane, heptachlor epoxide and para-BHC in 100% of all samples. That study was done on adipose samples taken from autopsies, and was from older subjects. A study of 4-year-olds in Michigan showed the presence of DDT in over 70%, PCB in 50%, and PBB in 13-21%. Nursing was the primary source of exposure for these children.
This multiple chemical load is due to several decades of chemical exposure from contaminated air food and water. Both outdoor and indoor airs are contaminated with chemicals. The EPAs TEAM study has documented the following chemicals as ubiquitous in the air:
* p-xylene
* tetrachloroethylene
* ethylbenzene
* benzene
* 1,1,1-trichloroethane
* o-xylene
Those listed as "often present" were:
* chloroform
* carbon tetrachloride
* styrene
* p-dichlorobenzene
This study found that air samples; taken with a personal monitor attached to the study individuals showed higher levels of chemicals in the "personal" air space over a 24-hour period than in outdoor air samples. These elevated personal levels and elevated breath levels were more directly attributable to indoor air pollution. However, they did note that persons who visited a service station or a dry cleaner had elevated personal breath levels of the solvents, as well as those who smoked and drove a vehicle during the day. They also found that certain occupations, such as chemical manufacturing, painting, and plastic manufacturing, caused higher levels of exposure.
Testing for chemical residues on food has been routinely employed throughout the world. None of the studies has found food sources free of contamination. On the contrary, multiple contaminants are usually found. The most comprehensive for the United States is the ongoing FDA Total Diet Survey. While the Total Diet Survey looked for the presence of many different chemicals, their findings for chlorinated pesticides are alarming. For example, DDE was found in 63% or more of the 42 foods sampled. Since DDT and DDE have been banned from use in the US since 1972, it is likely that some of this contamination is from produce imported form other countries where it is still used.
Unfortunately, since toxic chemicals are ubiquitously used throughout the world, they move easily around the globe on the winds. Unless these pesticides are trapped in the soil, tree bark, or other stable materials, persistent volatile pesticides, including DDT and toxaphene, begin a wind-driven leapfrogging around the globe. The more volatile the chemical, the faster it hops and the less readily it enters the fat of any plant or animal it contacts. Volatile chemicals applied in tropical regions evaporate into the atmosphere and then condense in cooler climates. As the ambient temperature falls, the compound becomes less volatile, so the periods between hopping of a compound from one place to another tend to lengthen. So, if two forests were exposed to identical amounts of a volatile pesticide, trees in the colder climate would become more heavily contaminated.
DDT and DDE are less volatile than solvents and do not leapfrog as well, and so tend to stay where they land and may be there for a year before jumping again. This global leapfrogging can account for one alarming study of the diet of Arctic indigenous women. The diets of two groups of women from the eastern and western Canadian Arctic were found to be very high in organochlorine compounds (OCC). The primary sources of these compounds were the meat and blubber of ringed seal, walrus, mattak and narwhal, as well as caribou, whitefish, inconnu, trout and duck. Since these OCCs were transported in the air, they landed in the arctic, but due to the low temperature were unable to volatize again and leapfrog away.
While there is virtually no debate left about whether our world is polluted or not, there is a considerable amount of debate as to whether or not these environmental toxins have adverse health effects on humans. Enough evidence of a positive association between chemical exposure and disease exists to document that a serious problem exists and that caution is urged. An article published in JAMA in 1994 entitled Decreasing Cardiovascular Disease and Increasing Cancer Among Whites in the United States from 1973 through 1987, Good News and Bad News, showed that while heart disease was declining, cancer mortality for men and women born after 1940 was much higher than for previous generations. These cancers were not linked to smoking, but were relegated to other environmental factors. For men the rate of cancer was 200% of that of previous generations, and for women the rate was 50% higher. Not only are cancer rates rising, but there is currently an alarming rise in the incidence of asthma, especially among children throughout the world. These incidents appear to be associated with ambient pollution levels. Much has also been said about the estrogenic effect of certain environmental chemicals and the devastating effect upon wildlife, and possibly humans as well. There is, therefore, much evidence to indicate that several chronic health problems appear to be related to environmental chemicals. Three of the known effects--immunotoxicity, neurotoxicity and endocrinotoxicity will be covered.
Environmental chemicals have a wide range of damaging effects on the function of the immune system. These range from decreased cell-mediated immunity (with a decrease in infection and tumor fighting) to increased sensitivity (allergy) and increased autoimmunity.
Among the organochlorine compounds (OCCs), DDT has been found to have many damaging effects on the immune system:
* reduced killing capacity of PMNs
* reduced number of plasma responder cells
* increased degranulation of mast cells
* leucopenia
* decreased phagocytic ability
* changes in the spleen, thymus, and lymph glands
* variation in complement
* disturbances in fetal and perinatal immune regulation
Similar effects have also been found after exposure to hexachlorobenzene (HCB) and the chlordanes (also OCCs). Hexachlorobenzene is a chlorinated pesticide used as a fungicide. It is also found to be present in chlorinated solvents such as perchloroethylene, which is used in dry cleaning and is very elevated in individuals from Western Europe. Chlordanes were primarily used as termiticides in the US and Canada until 1978 when they were banned from use in the home. They are still used on certain crops and in some seed treatment.
Studies of thousands of patients at the Environmental Health Center-Dallas have shown that persons with two or more OCCs present in their serum have some form of immunotoxicity.
The chemicals produced by combustion, the polycyclic aromatic hydrocarbons (PAHs), have been shown to have similar inhibiting effects on the immune system, including:
* decreased T-cell-dependent antibody response
* decreased splenic activity
* diminished T-cell effector functions
* suppression of T-cytotoxic induction
* lower natural killer cell activity
They are also highly carcinogenic.
The organophosphate pesticides (OPs), which are not as biologically persistent as the OCCs, are also toxic to the immune system. They have been found to cause decreased percentages of CD4 and CD5 cells, increased number and percentages of CD26 cells, increased incidence of atopy and antibiotic sensitivity, and high rates of autoimmunity. This elevation in autoimmunity is reflected by high levels of antibodies to smooth muscle, parietal cells, brush border, thyroid, myelin and elevated ANA. Similar immunosuppression is also found for the organotins and for the heavy metals.
The mode of exposure to the pesticide appears to have an effect on the persistence of immunotoxicity, as demonstrated by polybrominated biphenyl (PBB) spills. Exposed individuals were found to have lower levels of circulating T-lymphocytes and reduced lymphoproliferation response, resulting in reduced cell-mediated immunity (CMI). They also had a high prevalence of persistent skin, neurological and musculoskeletal symptoms. These changes have persisted through all studies. This indicates that when these toxins are concentrated in the food chain before reaching humans, their effect is longer lasting.
The development of autoimmunity has been linked with chemical exposure as well. The notion of chemically-induced autoimmune states is not new; since many chemicals are known to induce the onset of systemic lupus erethematosis (SLE). Some chemicals, like formaldehyde and other volatile organic compounds, are thought to induce tissue-specific autoimmune reactions by acting as haptens. These low-molecular-weight molecules will bind to various tissues in the body, making a new antigenic combination. The immune system then makes an antibody to this new combination which can attack the parent tissue with or without the chemicals being present. Chemically exposed individuals will often present with elevated antibodies to certain body tissues, including anti-myelin, anti-parietal, anti-brush border, and anti-smooth muscle.
Washing dishes by hand with an antibacterial dishwashing liquid can do more than just ensure that the plates, glasses, and silverware are free from grease and germs, according to Peter Vikesland of the Virginia Polytechnic Institute and
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New research shows that the triclosan in anti-bacteria dishwashing soaps may react with chlorinated drinking water to produce levels of chloroform that exceed EPA regulations. Because of its antibacterial, antifungal, and antiviral properties, triclosan is found in toothpastes, acne creams, deodorants, lotions, and hand soaps. It is also incorporated into a wide range of consumer goods, including kitchen tiles, children’s toys, cutting boards, toothbrush handles, hot tubs, and athletic clothing. As triclosan flows down drains, it is making its way into surface waters and sewage treatment plants, the bile of fish, and breast milk, according to the
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The formation of chloroform from triclosan is of concern because the
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The reaction of phenols such as triclosan with free chlorine is well known, but Vikesland’s research is important because “it ties the use of a household product to increased exposure to a disinfection byproduct,” says David Sedlak, a professor in the civil and environmental engineering department at the
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Since writing the paper, Vikesland’s team has conducted follow-up research under conditions that more closely mimic those found during home dishwashing. The new experiments used EPA’s maximum allowable residual disinfectant concentration of 4 milligrams per liter in tap water and were conducted at 40° C, which fits well with the cleaning recommendations of the Soap and Detergent Association. (The association’s website says that dishwater temperatures of less than 33° C, even with sufficient detergent, are likely to leave a greasy film, while the hottest water most people’s hands can tolerate is about 43° C.)
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Under these conditions, triclosan reacts with free chlorine to generate more than 50 parts per billion (ppb) of chloroform in the dishwater. When combined with the other trihalomethanes in the water, the additional chloroform could easily ratchet up the concentration of total trihalomethanes to 80 ppb, which is EPA’s maximum allowable amount, or higher, Vikesland says.
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“Since chloroform and other trihalomethanes and disinfection byproducts are already likely to be present in the tap water, and since chloroform, the other THMs, and many other disinfection byproducts are highly volatile, there is a very real likelihood that washing dishes with triclosan-containing liquid could cause additional and troubling significant exposure to these volatiles through inhalation and potentially through dermal absorbtion,” says Erik D. Olson, senior attorney for the Natural Resources Defense Council, a nonprofit environmental group. Olson calls the research “significant.”
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Water treatment plants are working hard to keep the levels of trihalomethanes in tap water below 80 ppb, Vikesland says, noting that the admissible level has recently decreased from 100 ppb. If there is any bromide in the water, the level of trihalomethanes produced during dishwashing is likely to shoot up even higher, he says.
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The research makes clear that it is always wise to wear gloves when dishwashing, says Doris Day, M.D., an assistant professor of dermatology at
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Vikesland’s research also shows that triclosan’s reaction with free chlorine produces a number of chlorinated triclosan intermediates, including 2,4 dichlorophenol. In the presence of sunlight, these chlorinated intermediates could be producing dioxins, say McNeill and his colleague, William Arnold of the
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It is unlikely that such dioxins would be generated during dishwashing even near a window on a sunny day because the glass would screen out most of the ultraviolet light necessary to produce the dioxin. But the research suggests that dioxins could be forming near swimming pools in some situations. “There’s triclosan in hand soaps and moisturizers. If someone who has triclosan-containing moisturizer on jumps into the pool … they’re a potential source for chloroform and chlorinated dioxin formation,” Vikesland says. The same is true for a child using an antimicrobial soap before getting into the pool, McNeill and Arnold agree. “You could produce a dioxin on the surface of your skin that gets absorbed through the skin,” Sedlak adds.
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McNeill and Arnold say that the research also calls for more detailed studies of whether chlorinated triclosans are being released from wastewater treatment plants. Because triclosan is widely found in the environment, chlorinated triclosan could be a source of toxic dioxins in the environment, says
As mentioned earlier, a study showed that men born in the 1940s had twice as many cancers as those born in 1888-1897, and more than twice as many cancers not linked to smoking. Women born in the 1940s had 50% more cancers, and 30% more cancers not linked to smoking (whites).
Breast Cancer
One of the cancers that has a very clear association with environmental chemicals is breast cancer. Three studies have shown elevated levels of different OCCs in the adipose tissue of breast cancer patients as compared with controls. The chemicals found to be higher in the women with malignancies were DDT, DDE, PCBs and HCH (hexachlorocyclohexane; known as Lindane or BHC, a chlorinated pesticide that is still commonly used to treat lice infestations (Kwell shampoo)). Not only are they higher in the adipose tissue of breast cancer patients, but they are actually found in higher concentrations in adjacent healthy tissue. Serum levels of OCCs have also been associated with an increased risk of breast cancer. Elevated levels of DDE and PCB in serum can indicate a fourfold increased risk of breast cancer compared with normal risk. Individuals with breast cancer often have both higher levels and greater numbers of individual OCCs than other patients.
Childhood Cancers
Childhood cancers have also been evaluated for epidemiological association with chemical exposure. In one study, 45 childhood brain cancer patients were compared with 85 friend controls. A significant positive association was found between brain cancer and exposure to no-pest strips, termite treatment, Kwell shampoo (Lindane) flea collars on pets, diazinon use in the garden or orchard, and the use of herbicides in the yard. When compared with 108 controls, a significant positive association was found with pesticide bombs in the home, termite treatment, flea collars on pets, insecticide use in the garden, carbaryl in garden, and herbicide use in the garden.
Several other studies of childhood chemical exposures found the following associations:
* 2,4-D (a common weed killer) used around the home associated with soft tissue sarcomas
* no-pest strips in the home associated with leukemia
* insecticide use in the home associated with brain tumors for those aged <20
* household pesticide use associated with leukemia
* household insecticide use associated with non-lymphocytic leukemia
2,4-D, a chlorophenoxy acid herbicide, gained notoriety from its combination with 2,4,5-T to form a mixture known as Agent Orange. It is commonly used by municipalities and states to spray roadways and rights-of-way to keep the weeds down. It can be purchased at home stores for home lawn care and is often applied by chemical lawn care companies. It contains several dioxin contaminates and is quite toxic to animals, children and adults.
For adults, the use of chlorophenoxy acid herbicides (2,4-D) has been strongly associated with an increased incidence of lung cancer, stomach cancer, leukemia, Hodgkin's lymphoma (two studies found a five-fold increased risk), non-Hodgkin's lymphomas (NHL) (five-to six-fold increased risk), and soft tissue sarcomas (many studies have found five- to seven-fold increased risk, with one review study finding a 40-fold increased risk). One study showed Kansas farmers having a six-fold increased risk of lymphomas and soft tissue sarcomas in persons using it 20+ days/year compared with non-exposed individuals. Those who mixed and applied herbicides and were exposed 20+ days/year were eight times as likely to contract NHL.
Factors associated with increased risk of NHL from 2,4-D exposure are:
* increased period of time of exposure
* not using protective equipment
* using backpack or hand sprayers
* employing tractor-mounted or mist blower sprayer
* applying herbicides aerially
Hematologic Malignancies
Several studies have associated exposure to solvents with acute myelogenous leukemia (AML), multiple myeloma, and other forms of leukemia. A study of 14,457 workers that were exposed to trichloroethylene between 1952 and 1953 showed that mortality was increased for multiple myeloma and NHL in white women. In a Finnish study, workers exposed to 1,1,1-trichloroethylene showed excess cancers of the cervix, uteri and lympho-hematopoietic tissues. After 10 years (from the first measurement), excess pancreatic cancer and NHL were seen. At a 20-year follow-up, excess multiple myeloma and cancer of the nervous system were found. Workers exposed to trichloroethylene showed an excess of cancers of the stomach, liver, prostate, and lympho-hematopoeitic tissues.
There have been at least 280 cases of aplastic anemia associated with pesticide exposure reported in the literature. The majority of these cases were young (average age 34) with a short latency (mean, 5 months) and had a history of occupational exposure to pesticides. Another study which looked at the cancer risk for painters showed increased cancer rates for multiple myeloma, bladder tumors, as well as kidney and other urothelial tumors. A study in Sweden of 275 confirmed diagnoses of multiple myeloma. This study revealed that exposures to chlorophenoxy acid herbicides (2,4-D) and DDT were prime risk factors.
The nervous system is a particularly sensitive target for toxic agents for several reasons. Besides the nervous system being such a good target, there are powerful neurotoxic agents available to attack it. Most of the major classes of pesticides kill pests by attacking their nervous system. They are neurotoxins by design. The OCCs affect the nerve by disrupting the ion flow along the axon. The OPs, which came out of nerve gas research, and carbamates affect acetylcholinesterase resulting in excessive acetylcholine levels in the synapses. Solvents, some of which were originally used as anesthetics, dampen the propagation and transmission of electrical impulses along the nerve axons. All of these agents produce various forms of toxic encephalopathy (either acute or chronic, selective or diffuse toxic encephalopathies), as neuronopathies, axonopathies, myelinopathies or vasculopathies.
Neuronopathies
Neuronopathies can be diffuse or selective, depending on whether specific neurons are affected, or if the damage is more broadly spread throughout the nervous system. The target site of toxic agents producing neuronopathies is the nerve cell body, with the consequence of either axonal or dendritic breakdown. An example of a neurotoxin causing diffuse neuronopathy is methylmercury (amalgam fillings) which preferentially damages the granule cells of layer IV in the visual cortex, granule cells in the granular layer of the cerebellum and the sensory neurons of the dorsal root ganglia. This brings about neuronal degeneration, progressing to necrosis with axonal dystrophy and demyelination. Another is aluminum which causes fatal dialysis encephalopathy following 3-7 years of intermittent dialysis.
The neuronopathies can also be selective, affecting only certain neurons. Examples of agents causing selective neuronopathies would include adriamycin, which affects the dorsal root ganglia; cisplatin, which affects sensory neurons; and manganese (metal fume fever), which produces a Parkinson-like syndrome. Manganese-induced damage is found in the substantia nigra, globus pallidus, and caudate nucleus, with depletion of dopamine and serotonin levels. Symptoms begin with psychiatric changes followed by impaired motor activity with muscle rigidity and tremors. Parkinsonism is also caused by MPTP, a contaminant found in synthetic heroin. This compound has brought on sudden Parkinson-like symptoms rapidly after exposure to the heroin. MPTP is metabolized in monoamine-oxidase (MAO) containing tissues to MPP+, the ultimate neurotoxin to MAO-containing tissues, which is selectively toxic to substantia nigra cells. It effectively blocks dopamine production.
Axonopathies
Axonopathies are differentiated by the area of the axon that is affected. The proximal axon is different in its ability to initiate action potentials and to synthesize protein. Damage to this part of the axon is referred to as proximal axonopathy. This is the type of damage seen in amytrohic lateral sclerosis (ALS). Proximal axonopathies are often caused by volatile organic compounds--e.g. halomethane, methylene chloride, carbon tetrachloride, and butane--all of which decrease the excitability of the neuron by stabilizing membranes and decreasing ion flux. Distal axonopathies have been shown to be caused by a variety of compounds including acrylamide (a polymerizing agent to strengthen paper) which primarily affects sensory fibers, and carbon disulfide (a solvent for fats and lacquers and for extraction of oil from olives, palmstones and other oil-bearing fruits) which produces distal axonopathy to both sensory and motor fibers. It also decreases norepinephrine levels. Hexacarbon solvents lead to multifocal distal progressive sensorimotor axonopathy with giant axonal swelling. Paranodal demyelination of swollen axons occurs frequently with exposure to these solvents.
The group of compounds that causes distal axonopathies also includes the organophosphate pesticides (OPs) (parathion, malathion, diazinon, etc.) and the carbamates. OPs cause acetylcholinesterase enzymes to be phosphorylated. Exposures may be additive and the effects may last until more acetylcholinesterase is synthesized. Carbamates (carbaryl, sevin, aldicarb) cause the acetylcholinesterase to be carbamylated. This is not a stable bond, and is hydrolyzed fairly easily.
Myelinopathies
Myelinopathies are caused by the organotins, which are used as stabilizers in plastic polymers and catalysts in silicon and epoxy curing. They are also used in wood and textile preservation as fungicides, bactericides and insecticides. Examples of the organotins are TET and TMT. Hexachlorophene (HCP) added to soaps for antimicrobial action also causes damage to the myelin. It is readily absorbed through intact skin and mucous membranes. Like TET and TMT, it causes blurred vision and muscular weakness progressing to paralysis. The optic nerve is also sensitive to particular solvents, such as toluene, CS2, and benzene. Other solvents can lead to specific myelinopathies, as the trigeminal nerve is especially sensitive to trichloroethylene (found in dry cleaning fluid). Hearing loss is commonly caused by toluene, styrene, xylene, and trichloroethylene, which causes myelin damage to the vestibulococchlear nerve. Other toxins, such as carbon monoxide and cuprisone (a copper chelating agent used in the treatment of Wilson's disease), are examples of toxins affecting the maintenance of myelin.
Lead, a well-known neurotoxin, brings about encephalopathy by causing vascular changes leading to neuronal degeneration and necrosis as well as by causing neuronal degeneration itself. Early stages of plumbism include headache and nausea. Demyelination of motor nerves is also seen with lead.
With the exception of the rodenticide Vacor, agents that affect endocrine function, other than reproduction, tend to be compounds with extensive effects on other organs as well (heavy metals, pesticides, solvents). It would be very unusual to find an endocrine disorder as the sole or primary manifestation of an environmental toxicity. The most common symptoms of toxic damage to the endocrine system are:
* sleep disturbances or changes in energy level or mood
* alterations in weight, appetite and bowel function
* sexual interest and function change; in females any menstrual change
* changes in temperature perception, sweating, or flushing
* alteration of hair growth and skin texture
Adrenal Gland
In addition to the well documented estrogenic effect of the OCCs, actual damage to the endocrine organs is also noticeable. Aliphatic compounds (3-6 carbons in length with electronegative groups in both ends) cause necrosis of zona fasiculata and zona reticularis of the adrenals, where the glucocorticoids are produced. OCCs and carbamates have caused histologic changes to these areas in animal models. Cadmium and carbon tetrachloride (CCL4) have both been shown to cause non-specific inhibition of steroidogenesis. Occupational lead workers showed decreased secretions of corticosteroids, both glucocorticoids (17-hydroxy) and androgenic steroids (17-keto). In these persons, the lesion was apparently at the hypothalamus/pituitary level because normal ACTH response was found with stimulation. Dioxins and Mirex (used to treat fire ants) cause direct suppression of glucocorticoid synthesis, resulting in hypoglycemia.
Thyroid
The thyroid is not immune to environmental toxins, as many chemicals can cause a reduction of both T4 and T3. Thiocyanates, perchlorates, and pertechnetates are all competitive inhibitors of iodine transport in the thyroid, causing decreases in T4 and T3 and an increase in thyroid stimulating hormone TSH. Compounds which inhibit the thyroid peroxidase needed in the second step of thyroid hormone synthesis include:
* thiourea
* thiouracil
* PTU
* Carbimazole
* Aniline derivatives
* PABA
* Substituted phenols like resorcinol
* Phloroglucinol
Iodide and lithium block thyroid hormone release from the gland itself. Depressed levels of thyroid function have been correlated with exposures to lead, mercury, carbon disulfide, and PBBs. Lead workers, a heavily studied population, appear to suffer from a decrease in thyroid, secondary to problems with the hypothalamus (TRF). In Michigan, PBB-exposed persons showed non-goitrogenic thyroid dysfunction. Less well documented, but suggested to adversely affect the thyroid, are:
* organophosphates
* carbamates
* OCCs
* Fungicides
* Food coloring
* PCBs
Inducers of hepatic cytochrome P450 like Phenobarbital, benzodiazepines, calcium-channel blockers, steroids, retinoids, chlorinated hydrocarbons, and polyhalogenated biphenyls will (in addition to inducing P450) cause alteration in thyroid structure, leading to reduction in T4. Besides causing reduced functioning, some compounds will also cause thyroid cancer. Polycyclic hydrocarbons, nitrosamines, and other compounds are initiators of thyroid carcinogenesis. A common component of permanent hair dye preparations, 2,4-diaminoanisole sulfate (2,4-DAAS), when fed at high doses, caused a 58% incidence of thyroid neoplasms in male rats and 42% in females, compared with 7-8% in controls.
Reproductive
The effect of environmental chemicals, especially the estrogenic OCCs, is well documented. While many are estrogenic by themselves, when combined together, their estrogenicity can increase by a factor of 1,600. Some combinations can also cause previously non-estrogenic compounds to become estrogenic. However, there are also non-estrogenic toxic effects of the OCCs on both male and female reproduction. High levels of OCCs in the serum have been strongly linked to infertility, stillbirths and miscarriages. Urban air pollution has been associated with reduced male fertility. While there appears to be a worldwide decline in the sperm levels of males, males who are organic farmers have very high sperm density. This gives rise to the supposition that exposure to environmental chemicals lowers sperm levels, and that avoidance of such chemicals may help to bring the levels back up. There have been multiple studies on one OCC that is used agriculturally--dibromochloropropane (DBCP)--looking at its effect on sperm levels. These studies have demonstrated that exposure to DBCP leads to azospermia, and severe oligospermia. This may be only associated with DBCP or it may serve as a model of other OCC-induced spermatogenesis problems.
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