Module 2: Toxin Exposure Among Children

Introduction: Toxic Chemicals

Chemicals surround us. Today, there are over 80,000 chemicals in commerce, 15,000 of which are used in high volume in the United States.(1) In fact, there are more than 1,000 chemicals in just one cup of coffee.(2) Both natural and synthetic chemicals are used as pesticides, made into fibers for clothing, synthesized into medicines, and manipulated to build furniture, technological devices, and more. We are becoming increasingly reliant on chemicals; in 1918, the U.S. produced a total of 10 million pounds of synthetic chemicals. Today, the U.S. produces over 300 billion pounds of chemicals per year.(3) An average American makes and/or uses more than 1,500 pounds of chemical products per year.(4)

Chemicals, both natural and synthetic, have the potential to cause disease. Adverse health effects occur when toxic pollution is inhaled or ingested. At any instant, toxic pollution affects over 100 million people worldwide, shortening the average life span by 12.7 years.(5) In fact, 20% of all deaths in developing nations are caused by environmental pollution.(6)

While toxins threaten everyone’s health, infants and children are especially sensitive to toxins. This is because children are more exposed to chemicals (pound-by-pound), their organs are still developing, and their bodies are less able to detoxify. Children are also more vulnerable to toxins because they lack a fully developed blood-brain barrier, the structure in the central nervous system that prevents the passage of chemicals between the bloodstream and the neural tissue. In fact, a human brain continues to develop until age 20.(7) Children today are exposed to an ever-increasing number of chemicals, many of which have not been tested for their possible toxicity. Thus, we must be especially careful to shield children from these environmental toxins.

The World’s Toxic Top 10(8)


Examples of Toxins

Heavy Metals

Heavy metals are elements with high atomic masses. Heavy metals may be toxic; these toxins include arsenic, lead, mercury, and cadmium. Other heavy metals are necessary to life, including zinc, cobalt (found in vitamin B-12), and iron (found in hemoglobin). Furthermore, trace elements, such as copper, manganese, selenium, chromium, and molybdenum, are important to the human diet.(9)


Arsenic is number one on the 2011 Priority List of Hazardous Substances created by the Agency for Toxic Substances and Disease Registry (ATSDR). The National Priorities List (NPL) ranks the substances most commonly found at sites on the NPL, most of which are in America.(10) Arsenic is an element found naturally in soil, and often combines with other elements to form inorganic arsenic compounds. Well known for its use as a poison, arsenic is also used in wood preservatives, pesticides, and semiconductors. As a result, arsenic is found in the environment. Background exposure to arsenic in air is less than 0.1 micrograms per cubic meter (µg/m3) and in drinking water is less than 5µg/L; people exposed to arsenic in contaminated drinking water or workplace air receive more arsenic. Studies in the 1960s found that inorganic arsenic is a human carcinogen; since the U.S. Safe Drinking Water Act of 1975, nearly all pesticides based in inorganic arsenic compounds have been banned or pulled from the market. Beginning in December 2012, the EPA is also phasing out the use of organic arsenic compounds, which are considered less toxic than inorganic arsenic, and are found on sod farms and golf courses.(11)

Arsenic poisoning in drinking water threatens the health of people globally. Some of the most serious cases of arsenic-contaminated groundwater have been found in aquifers in Asia (in Bangladesh, China, India, and Nepal) and South America (Argentina and Mexico). Ingestion of 70-180 mg of inorganic arsenic can cause death. Other acute effects of arsenic ingestion include difficulty breathing and swallowing, intestinal pain, vomiting, diarrhea, muscle cramps, and severe thirst.(12) Symptoms of chronic arsenic poisoning, often due to drinking contaminated water, include garlic breath, extreme perspiration, muscle tenderness, changes in skin pigmentation, anemia, reduced sensation in the extremities, and peripheral vascular disease.(13) Inorganic arsenic is a human carcinogen, according to the Department of Health and Human Safety (DHHS), the EPA, and the International Agency for Research on Cancer (IARC);(14) however, inorganic arsenic does not induce cancer in laboratory rats.(15) Specifically, studies have shown that ingestion of inorganic arsenic increases risk of skin, liver, bladder, and lung cancer, while inhalation of inorganic arsenic increases risk of lung cancer.(16)(17) Therefore, the WHO and EPA set current limits for arsenic in drinking water at 0.01 parts per million (ppm) and OSHA limits arsenic exposure in workplace air at 10 micrograms per cubic meter of air (10 μg/m³) for 8 hour shifts and 40 hour work weeks.(18)

Arsenic poisoning in drinking water in Bangladesh and West Bengal, India, is considered by some to be the worst mass poisoning in history.(19) Millions of wells were dug throughout Bangladesh and West Bengal in the 1960s and 1970s, but they were not tested for metal impurities until they were contaminated with arsenic. As a result, around 75 million people in affected regions of Bangladesh and India are now subject to arsenic-contaminated water, and 200,000 to 270,000 deaths due to arsenic-induced cancer are expected in the future. A random survey conducted in 2001 of 3,208 groundwater samples in India and Bangladesh from shallow aquifers (less than 150 meters deep) found that 46% of the samples contained more than 10 μg/L of arsenic.(20) Efforts to reduce contaminated drinking water are hampered by the poverty of most Bangladeshis (annual per capita income of $370) and of the government’s lack of resources. Furthermore, exactly how arsenic leaches into the water is not clear, making the issue more difficult to solve. For now, the best approach is to treat contaminated groundwater after it is drawn (which is too expensive for most people in West Bengal and Bangladesh) or to let water sit out for a while so that inorganic arsenic can be converted into less harmful organic arsenic.(21)


Lead is second on the 2011 ATSDR Priority List of Hazardous Substances. Lead is a naturally occurring metal found in the Earth’s crust. In the past, lead has been used in the manufacture of gasoline, paints, ceramics, caulking, and solder pipe, but is no longer used to make these materials due to lead’s harmful health effects. For example, leaded gasoline was phased out beginning in 1973, and leaded household paint was banned in 1978.(22) Because of these regulations, levels of lead in the blood of American children have dropped by 86% since the late 1970s from a median level of 15 µg/dL in 1976 (before regulations were passed and enforced) to a median level of 1.9 µg/dL in 1999.(23)(24) However, lead is still used today in the manufacture of many products, including batteries, ammunition, metal pipes, and devices to shield X-rays.(25)

Although lead has many useful applications, it is known to cause health complications that affect almost all human organs. These complications include impaired intellect, memory loss, nerve disorders, infertility, mood swings, and problems with the cardiovascular, skeletal, kidney, and renal systems in adults. Lead can enter the body through ingestion or inhalation. Adults must be exposed to much more lead (compared to children) in order to suffer sustained health consequences. Most adults receive lead poisoning from work, especially in occupations related to welding, renovating, manufacturing car batteries, and maintaining bridges and water towers.(26) Children are exposed to lead in the form of dust and chips from deteriorating lead paint on the interior surfaces of older homes (built before lead paint was banned).

Children are most vulnerable to lead poisoning. In fact, two-year olds have the highest blood level concentration of lead, partly because they place many objects and toys, some laden with lead, in their mouths.(27) Children with blood-lead concentrations greater than 10 micrograms per deciliter (µg/dL), or one millionth of a gram of lead in about half a cup of blood, have excess lead exposure. Recent studies, however, have shown that children with blood-lead concentrations of even less than 10 µg/dL are subject to adverse health effects.(28) Lead poisoning has been shown to cause cognitive impairment (decreased IQ) in children globally.(29) A study comparing blood-lead concentrations and IQ in 172 children found that each increase of 10 µg/dL in the lifetime average blood-lead concentration was correlated with a 4.6 point decrease in IQ. In a subsample of children with maximal lead concentrations below 10µg/dL, a given change in lead concentration caused an even greater change in IQ.(30) In addition to lowering IQ, lead exposure also causes behavioral problems in 5- to 7-year-old children who were first exposed to dangerous levels of lead when they were 1-2 years old.(31) Children exposed to lead poisoning scored worse on a behavior test for opposition, hyperactivity, and attention deficit hyperactivity disorder (ADHD) than did their peers.


Mercury is third on the 2011 ATSDR Priority List of Hazardous Substances. Elemental mercury is found naturally as an odorless, shiny liquid metal. Toxic mercury vapors can be released naturally (from volcanic eruptions and from the earth’s crust) or synthetically (from waste incineration, coal combustion in power plants, automobile emissions, and disposal of industrial waste).(32) Mercury has been used to make thermometers, barometers, and fluorescent light bulbs. Mercury released into the air settles into water or on land, where it deposits and is converted (by microorganisms) into methylmercury, a highly toxic form of mercury that builds up in fish. Therefore, people can be exposed to mercury by ingesting fish that contain mercury, inhaling mercury vapors, or touching mercury.

Mercury exposure can damage the brain, heart, kidney, lungs, and immune system. There are three different chemical forms of mercury: elemental mercury, organic mercury (primarily methylmercury), and inorganic mercury compounds, each of which causes different health effects. Elemental mercury, usually inhaled as vapors and found in thermometers, can cause mood swings, irritability, nervousness, insomnia, headaches, muscle twitching/tremors, and decreased cognitive functions. Organic mercury, or mercury covalently bound to carbon, impairs neurological development in fetuses, infants, and children, since methylmercury can pass from mother to fetus through the placenta. Inorganic mercury, or mercury bound to inorganic compounds, often causes skin rashes, inflammation and, if ingested, diarrhea.(33) Blood-mercury levels in non-exposed people should be less than 2 µg/dL, and urine-mercury levels for a non-exposed person should be less than 20 µg/L.(34)

Many people are concerned with mercury levels in fish. In 1997, the Environmental Working Group (EWG) found that fish from over 1,660 U.S. waterways contained too much mercury to be safe for consumption. Soon after, the EPA confirmed that more than 1.6 million women and children were at risk of mercury contamination from fish. In 2004, the EPA and FDA issued warnings limiting fish consumption during pregnancy to 12 ounces per week. The EPA and FDA recommendations targeted pregnant women because fetuses are especially vulnerable to mercury poisoning. In 2006, the EWG initiated a Human Toxome Project (HTP) to define the full scope of industrial pollution. The HTP found methylmercury in 72 of the 73 people tested.(35) Some fish contain dangerous levels of mercury for all people. All people should avoid eating the four types of fish containing the highest levels of methylmercury: shark, king mackerel, swordfish, and tilefish.(36)

The disaster in Minamata Bay, Japan, is an example of a mercury outbreak. In 1908, the Chisso Corporation opened up a chemical factory in Minamata. The waste products from the plant were released into Minamata Bay. In 1925, the Chisso Corporation continued dumping untreated waste (containing methylmercury) into the bay, and, in exchange for damaged fisheries, paid fishermen for their losses. Not until the mid-1950s did people realize that some had developed a “strange disease,” now referred to as the Minamata disease. Victims of the Minamata disease had degenerate nervous systems, numbness in the limbs, muscle weakness, narrowing of the field of vision, and hearing and speech impairment (the same symptoms of methylmercury poisoning). Others died of the disease. In 1973, after many village protests, Chisso agreed to compensate victims and their families financially.(37)

“Developmental Delay in Cognitive Function for Each 10-Fold Increase in Prenatal Exposure to Mercury”(38)



Carcinogens are substances and exposures that can lead to cancer. Some carcinogens cause cancer by directly creating mutations in the DNA; others disrupt cell growth, thereby allowing some cells to grow uncontrollably. There are many known carcinogens that affect humans, including acetaldehyde, aflatoxins, asbestos, benzene, formaldehyde, hepatitis viruses, ionizing radiation, plutonium, radionuclides, radon, tobacco, and ultraviolet radiation.


Asbestos is the category of minerals present in nature as bundles of fibers that can be mined and then separated into thin, durable threads. These fibers are resistant to heat, chemicals, and fire, and do not conduct electricity. Therefore, asbestos fibers are commonly used for a variety of manufactured goods, including roofing shingles, ceiling and floor tiles, paper and cement products, textiles, and coatings. Asbestos minerals are classified into two major groups: serpentine asbestos (which have long, curly fibers that can be woven) and amphibole asbestos (which have straight, needle-like fibers that are more brittle and less able to be woven).(39)

Asbestos is carcinogenic, and is a health hazard when inhaled. When products containing asbestos are disturbed, tiny asbestos fibers are released into the air. Once inhaled, these tiny fibers may remain trapped in the lungs for a long time, scarring and inflaming the tissues, thereby disrupting breathing and causing long-term health problems.(40) Diseases from asbestos exposure take a long time to develop; cases of lung cancer or asbestosis may be diagnosed 15 years after a person’s initial exposure to asbestos. The three major health effects of asbestos exposure are:

  1. Asbestosis: a progressive, non-cancerous disease of the lungs. Asbestos fibers scar the respiratory tissues, making it more difficult for oxygen to enter the bloodstream. Symptoms include shortness of breath and a dry, crackling sound when inhaling. There are no effective treatments for asbestosis.(41)
  2. Lung cancer: a malignant tumor that invades and then obstructs the air passages in the lungs. Scientists believe that asbestos fibers kill cells, but while doing so, the dying cells release a protein (high-mobility group box 1 protein, HMGB1) that triggers the release of mutagens and growth factors that cause tumor formation.(42) Symptoms of lung cancer include coughing, difficulty breathing, shortness of breath, persistent chest pains, hoarseness, and anemia. People working in the milling, asbestos manufacturing, and mining industries have a higher risk of developing lung cancer than do people in other industries.(43)
  3. Mesothelioma: a rare form of cancer found in the membrane (thin lining) of the lung, chest, abdomen, and heart. Most mesotheliomas have been linked to asbestos exposure.(44)

Endocrine Disruptors

An endocrine disrupting compound is defined by the EPA as “an exogenous agent that interferes with synthesis, secretion, transport, metabolism, binding action, or elimination of natural blood-borne hormones that are present in the body and are responsible for homeostasis, reproduction, and developmental process.”(45) In other words, endocrine disruptors interfere with the functions and hormones of the innate endocrine system. Research has found that many endocrine disruptors are associated with early onset of puberty. Some synthetic endocrine disruptors include polychlorinated biphenyls (PCBs), plastics (bisphenol A), plasticizers (phthalates), pesticides (methoxychlor and DDT), fungicides (vinclozolin), and pharmaceutical agents (diethylstilbestrol). Some natural endocrine disruptors found in human and animal food include phytoestrogens (also known as dietary estrogen), such as genistein and coumestrol (found in soybeans, alfalfa, legumes, Brussels sprouts, and spinach).(46)

Bisphenol A (BPA)

Bisphenol A is a synthetic estrogen used in plastics manufacturing to harden polycarbonate plastics and epoxy resin. Polycarbonate plastics are used in food and drink packaging (water and baby bottles), compact discs, eyeglasses, computer and cell phone cases, impact-resistant safety equipment, and medical devices. Epoxy resins are used to coat metal products such as food cans, bottle tops, and water pipes.(47) The EWG estimates that approximately “6 billion pounds of BPA are produced annually globally, generating about $6 billion in sales.”(48)

BPA enters the body primarily through ingestion. BPA leaches from the epoxy can linings into canned foods. The degree to which BPA seeps from polycarbonate bottles into food and beverages depends on the temperature of the liquid or food, with more leaching occurring at higher temperatures. A 2007 study by the EWG showed that more than half of a random sample of canned foods, beverages, and canned infant formula sold in supermarkets in America contained detectable levels of BPA (at room temperature).(49) That explained the 2003-2004 CDC study that found detectable levels of BPA in 93% of 2,517 urine samples of a random sampling of people over six years old.(50)

In 2008, the NTP and the FDA concluded that current low levels of human exposure to BPA are safe in adults, but they were concerned about the potential health effects of BPA on the brain, behavior, and prostate glands of fetuses, infants, and children.(51) However, in 2010, the FDA announced its revised belief that trace BPA in food and beverages was no longer safe; consequently, it began encouraging industries to develop BPA-free can lining and bottles.(52)

“NTP conclusions regarding the possibilities that human development or reproduction might be adversely affected by exposure to bisphenol A. The NTP uses a five-level scale of concern:”(53)



Phthalates are a group of chemicals invented in the 1930s. Phthalates are used as plasticizers to soften and increase the flexibility of plastics (especially PVC plastic). Phthalates are also used in cosmetics, including perfume, hair spray, soap, shampoo, nail polish, and skin moisturizers. Phthalates were also present in pacifiers, soft rattles, and teething toys for babies until 1999. People are exposed to phthalates when applying cosmetics, eating food packaged in phthalate-coated plastic, drinking water containing phthalates, or breathing in phthalate dust from vinyl blinds, wallpaper, or flooring.(54) Children face an additional risk of exposure to phthalates from chewing on soft vinyl toys and other objects containing phthalates.

A study by the CDC in 2000 found high levels of phthalates in every one of 289 people tested.(55) Furthermore, levels of some phthalates in American women of childbearing age exceeded the levels determined by the government to be safe from birth defects.(56) A study conducted by the Mt. Sinai School of Medicine on phthalates in 6- to 8-year-old girls found phthalates in every one of the 90 girls tested.

Phthalates, so prevalent in our consumer culture, are known to be endocrine disruptors. High levels of phthalates have been linked to decreased sperm motility and concentration, damaged sperm DNA, and alterations in hormone levels in adult men.(57) In fact, a study in 2005 found significant differences in the reproductive systems of baby boys whose mothers had high phthalate levels during pregnancy. Phthalates do not only affect male reproductive systems, but also alter thyroid hormone levels and increase insulin resistance in adult men in the U.S.(58) Researchers also found that higher levels of prenatal exposure to two tested phthalates significantly increased the odds of motor delay. One of the phthalates correlated with significant decreases in mental development in girls, and prenatal exposure to three of the phthalates tested were significantly associated with more behavioral complications, such as heightened emotional reactivity, anxiety/depression, somatic complaints, and withdrawn behavior.(59) The biological mechanisms behind the effects of phthalates are still being explored.

In 2008, mounting pressure from the EWG and other health groups led to legislation banning six phthalates from children’s toys and cosmetics. Several retailers, including Wal-Mart, Toys-R-Us, Lego, Evenflo, and Gerber, said they would phase out toys containing phthalates.

Methyl isocynate

Methyl isocynate is a highly toxic, flammable, colorless liquid. It is used in the production of rubbers, adhesives, and pesticides. Methyl isocynate gas was present in the gas leak from a pesticide plant in Bhopal, India, on the night of December 2, 1984.(60) The 40 tons of leaked methyl isocynate gas killed over 3,800 people instantly and caused premature death for thousands more.(61) The Bhopal disaster illustrated the results of rapid industrialization in a nation where safety regulations were not keeping pace with industrialization. Public health infrastructure in Bhopal in 1984 was very weak; poor-quality tap water was accessible for only a few hours of the day, human waste was dumped into nearby lakes (a source of drinking water), the four hospitals in the city were all short on staff and beds, and there was no established mass casualty emergency response system.(62) Following the events of the Bhopal disaster, environmental awareness and activism in India increased significantly. For example, the Environmental Protection Act was passed in 1986, creating the Ministry of Environment and Forests (MoEF) to administer and enforce environmental policies.(63)

Environmental Teratogenic Agents

Teratogenic agents, or teratogens, are toxins that cause abnormal development, leading to birth defects. Of the 3-5% of American children born per year with birth defects, only 2-3% of them are considered to have teratogen-induced malformations.(64) Fetuses are most vulnerable to toxins during organogenesis, when the organs begin to develop (approximately 3 weeks post-conception). The type and severity of the birth defect are related to the duration of exposure and the specific teratogen. Teratogenic agents are classified as genetic or environmental. Genetic agents are changes in the genetic material of the fetus that are either inherited or newly acquired. Common environmental teratogenic agents include radiation, metals (such as methylmercury), thalidomide , ethanol (alcohol), nicotine, and cocaine.(65) These toxins harm the health of exposed mothers, but the damage is worse for their children who are prenatally exposed to these toxins.


Alcohol consumption causes approximately 79,000 deaths per year in America, making it the third leading cause of death attributed to lifestyle choices in the U.S.(66) For adults, immediate health risks of alcohol consumption include unintentional injuries (traffic accidents, falls), domestic violence , and miscarriage and stillbirth (among pregnant women). Long-term health effects include neurological problems (dementia, stroke, neuropathy), cardiovascular problems (hypertension), psychiatric problems (depression, anxiety), cancer (of the mouth, esophagus, colon, and breast), and liver diseases.(67)

Developing fetuses are especially vulnerable to alcohol exposure. Excluding abortion, Fetal Alcohol Syndrome (FAS) is the most serious consequence of alcohol consumption during pregnancy. FAS complications include abnormal heart structure, behavioral problems, mental retardation, facial structural problems, and slow growth before and after birth.(68) Studies show that prenatal exposure to alcohol causes children to suffer significant cognitive defects and behavioral problems due to the alcohol-related changes in brain structure (specifically, changes in the basal ganglia, corpus callosum, cerebellum, and hippocampus).(69) Children prenatally exposed to lower amounts of alcohol and children with FAS experience learning and memory deficits, behavioral problems (drug and alcohol abuse), hyperactivity, impulsivity, decreased sociability, and poor communication skills.(70)

Common Symptoms of Fetal Alcohol Syndrome(71)


Nicotine, an ingredient found in tobacco plants and used to make cigarettes and other tobacco products, is a highly toxic and addictive drug. Only 60 mg of nicotine is lethal to an adult, and smokers generally receive 1 mg of nicotine per cigarette smoked. Acute effects of nicotine poisoning for adults include nausea, vomiting, salivation, diarrhea, dizziness, confusion, and weakness. Higher levels of exposure to nicotine causes decreased blood pressure, difficulty breathing, irregular pulse, convulsions, respiratory failure, and death.(72)

Nicotine also affects the developing fetus; chronic prenatal nicotine exposure leads to reduced infant birth weight, attention deficit disorders, and other cognitive problems in children.(73) Studies using animal models found birth defects in rats exposed to nicotine, including decreased birth weight, increased infant mortality, delayed sensorimotor development, higher levels of anxiety, and changes in learning and memory(74)(75). Recent findings in humans confirm the teratogenic nature of prenatal tobacco exposure. Prenatal tobacco exposure affects speech processing, irritability, attention levels, ability to self-regulate, and response to novelty in infants.(76) 


Thalidomide, a sedative drug, was first widely used in the 1950s to treat morning sickness among pregnant women. In 1961, thalidomide was withdrawn after it was shown to cause birth defects.(77) Today, thalidomide is approved by the FDA for use in treating multiple myeloma (a cancer of the plasma cells in bone marrow) and erythema nodosum leprosum (skin lesions caused by leprosy).(78) Thalidomide is also widely used today in rural areas of the world that lack extensive medical surveillance initiatives.

Women who take just one dose of thalidomide during pregnancy may have a child with a birth defect. Symptoms of thalidomide include malformation of craniofacial structures and extremities (leading to shoulder weakness, hypoplasia), malformation of the ear (leading to hearing loss), ocular anomalies (glaucoma, refractive error), facial nerve palsy, defects in the central nervous system, and mental retardation.(79) Side effects of thalidomide for adults, other than birth defects, include peripheral neuropathy, blood clots, drowsiness, seizures, rash, headache, weakness, weight changes, constipation, dry mouth, and swelling of the hands, ankles, feet, or lower legs.(80)

Children with Thalidomide-Related Birth Defects at a Swimming Pool(81)


Go To Module 3: Environmentally-Related Infectious Diseases >>


(1) National Institute of Environmental Health Sciences (NIEHS). The New Environmental Health. Publication no. NIH Publication #02-5081. Research Triangle Park. Print.

(2) Ibid.

(3) Ibid.

(4) Ibid.

(5) Landrigan, Philip. "Vulnerability of Children to Environmental Assaults: A Global Perspective." Global Health & Innovation Conference. Session L2, New Haven. 21 Apr. 2012. Speech.

(6) Ibid.

(7) "Environmental Toxins." Lecture. Action Group Project. 2008-2009. NH Leadership. Web. 1 June 2012.

(8) Zimmerman, Jess. What Is Poisoning Us Today? Digital image. Grist. Grist Magazine. Web. 06 June 2012.

(9) Soghoian, Samara, and Richard H. Sinert. "Heavy Metal Toxicity." Heavy Metal Toxicity. Ed. Mark Louden, John T. VanDeVoort, John G. Benitez, John D. Halamka, and Asim Taraba. 6 May 2011. Web. 01 June 2012.

(10) "The Priority List of Hazardous Substances That Will Be the Subject of Toxicological Profiles." Agency for Toxic Substances and Disease Registry, 25 Oct. 2011. Web. 06 June 2012.

(11) "Health/Toxics: Arsenic in Treated Wood." Environmental Working Group, 2012. Web. 06 June 2012.

(12) Mergel, Maria. "Arsenic." Toxipedia, 12 May 2011. Web. 06 June 2012.

(13) Ibid.

(14)Arsenic. Publication no. 7440-38-2. ATSDR, Aug. 2007. Web. 6 June 2012.

(15) Mergel, Maria. "Arsenic." Toxipedia, 12 May 2011. Web. 06 June 2012.

(16) "Arsenic." American Cancer Society, 17 Feb. 2011. Web. 06 June 2012.

(17)Arsenic. Publication no. 7440-38-2. ATSDR, Aug. 2007. Web. 6 June 2012.

(18) Ibid.

(19) Mergel, Maria. "Arsenic Poisoning in Bangladesh." Toxipedia, 24 October 2010. Web. 06 June 2012.

(20) Appelo, Tony, and Jan P. Heederik, eds. Arsenic in Groundwater: A World Problem. Utrecht, The Netherlands: Secretariat Netherlands National Committee, IAH, 2006. Print.

(21) Mergel, Maria. "Arsenic Poisoning in Bangladesh." Toxipedia, 24 October 2010. Web. 06 June 2012.

(22) "Health/Toxics: Lead." Environmental Working Group, 2012. Web. 31 May 2012.

(23) Ibid.

(24) American Academy of Pediatrics Committee on Environmental Health. Lead exposure in children: Prevention, detection, and management. Pediatrics.2005; 116:1036–1046.

(25) "Toxic Substances Portal: Lead." Agency for Toxic Substances and Disease Registry. Web. 31 May 2012.

(26) NIEHS. Lead and Your Health. NIEHS. Web. 31 May 2012.

(27) In fact, two-year old children have the highest blood level concentration of lead, because they place many objects in their mouths, some of which can be contaminated with lead.

(28) NIEHS. Lead and Your Health. NIEHS. Web. 31 May 2012.

(29) Ibid.

(30) Canfield RL, Henderson CR Jr, Cory-Slechta DA, Cox C, Jusko TA, Lanphear BP. Intellectual impairment in children with blood lead concentrations below 10 micrograms per deciliter. N Engl J Med. 2003 Apr 17; 348(16):1517-26.

(31) Chen A, Cai B, Dietrich KN, Radcliff J, Rogan WJ. Lead exposure, IQ, and behaviour in urban 5-to 7-year olds: does lead affect behaviour only by lowering IQ? Pediatrics. 2007;119:e650–8

(32) "Mercury & Neurodevelopment." NIEHS, 14 Nov. 2011. Web. 31 May 2012.

(33) Davis, Charles P. "Mercury Poisoning." Ed. Wiliam C. Shiel, Jr. WebMD, 2012. Web. 31 May 2012.

(34) "The Health Effects of Mercury." New Jersey State Department of Health. Web. 31 May 2012.

(35) "Health/Toxics: Mercury." Environmental Working Group, 2012. Web. 31 May 2012.

(36) "Mercury Levels in Commercial Fish and Shellfish." FDA, 26 May 2011. Web. 31 May 2012.

(37) "TED Case Studies: Minamata Disaster." The Mandala Projects, 11 Jan. 1997. Web. 01 June 2012.

(38)Developmental Delay in Cognitive Function for Each 10-Fold Increase in Prenatal Exposure to Mercury. Digital image. NIEHS, 14 Nov. 2011. Web. 01 June 2012.

(39) National Cancer Institute. "Asbestos Exposure and Cancer Risk." National Institutes of Health. Web. 01 June 2012.

(40) Ibid.

(41) EPA. "Asbestos: Basic Information." Environmental Protection Agency, 25 May 2012. Web. 01 June 2012.

(42) Yang H., Rivera Z., Jube S., Nasu M., Bertino P., Goparaju C., Franzoso G., Lotze M. T., Krausz T., Pass H. I., Bianchi M. E., Carbone M. (2010). Programmed necrosis induced by asbestos in human mesothelial cells causes high-mobility group box 1 protein release and resultant inflammation. Proc. Natl. Acad. Sci. U.S.A. 107, 12611–12616. doi: 10.1073/pnas.0913004107.

(43) EPA. "Asbestos: Basic Information." Environmental Protection Agency, 25 May 2012. Web. 01 June 2012.

(44) Ibid.

(45) Diamanti-Kandarakis E et al. 2009 Endocrine-Disrupting Chemicals:  An Endocrine Society Scientific Statement.
Endocrine Reviews 30(4):293-342

(46) Ibid.

(47) "Since You Asked - Bisphenol A (BPA)." NIEHS, 30 Mar. 2012. Web. 01 June 2012.

(48) "Bisphenol-A." Environmental Working Group, 2012. Web. 01 June 2012.

(49) Ibid.

(50) "Since You Asked - Bisphenol A (BPA)." NIEHS, 30 Mar. 2012. Web. 01 June 2012.

(51) "Bisphenol A (BPA): Use in Food Contact Application.” US Food and Drug Administration, 30 Mar. 2012. Web. 01 June 2012.

(52) "Bisphenol-A." Environmental Working Group, 2012. Web. 01 June 2012.

(53)NTP Conclusions regarding the Possibilities That Human Development or Reproduction Might Be Adversely Affected by Exposure to Bisphenol A. The NTP Uses a Five-level Scale of Concern. Digital image. NIEHS, 3 Sept. 2008. Web. 01 June 2012.

(54) ToxTown. "Phthalates." U.S. National Library of Medicine. Web. 01 June 2012.

(55) "Water Pollution Caused by Cosmetic Chemicals, Cleaning Supplies and Plastics: » Phthalates." Environmental Working Group, 2012. Web. 01 June 2012.

(56) Ibid.

(57) Ibid.

(58) Ibid.

(59) Whyatt RM, Liu X, Rauh VA, Calafat AM, Just AC, Hoepner L, Diaz D, Quinn J, Adibi J, Perera FP, Factor-Litvak P. “Maternal prenatal urinary phthalate metabolite concentrations and child mental, psychomotor, and behavioral development at 3 years of age.” Environ Health Perspect. 2012 Feb; 120(2):290-5. Epub 2011 Aug 31.

(60) Broughton E. The Bhopal disaster and its aftermath: a review. Environ Health. 2005; 4:6.

(61) Ibid.

(62) Ibid.

(63) Ibid.

(64) Gilbert, Steven G. A Small Dose of Toxicology: The Health Effects of Common Chemicals. 2nd ed. Seattle: Healthy World, 2012. PDF.

(65) Ibid.

(66) CDC. "Alcohol and Public Health: Fact Sheets." Centers for Disease Control and Prevention, 28 Oct. 2011. Web. 04 June 2012.

(67) Ibid.

(68) Ibid.

(69) Mattson, Sarah N., Amy M. Schoenfeld, and Edward P. Riley. "Teratogenic Effects of Alcohol on Brain and Behavior." National Institute on Alcohol Abuse and Alcoholism (NIAAA). Web. 04 June 2012.

(70) Ibid.

(71)Fetal Alcohol Syndrome Symptoms Chart Picture. Digital image. Syndromespedia. Web. 04 June 2012.

(72) Gilbert, Steven G. A Small Dose of Toxicology: The Health Effects of Common Chemicals. 2nd ed. Seattle: Healthy World, 2012. PDF.

(73) Ibid.

(74) Schneider T, Ilott N, Brolese G, Bizarro L, Asherson PJ, and Stolerman IP. Prenatal exposure to nicotine impairs performance of the 5-choice serial reaction time task in adult rats. Neuropsychopharmacology. 2011 Apr; 36(5):1114-25. Epub 2011 Feb 2.

(75) Vaglenova J, et al. Long-lasting teratogenic effects of nicotine on cognition: Gender specificity and role of AMPA receptor function. Neurobiology of Learning and Memory. 2008; 90(3):527–536.

(76) Cornelius MD, Day NL. Developmental consequences of prenatal tobacco exposure. Curr. Opin. Neurol. 2009; 22:121–125.

(77) Gilbert, Steven G. A Small Dose of Toxicology: The Health Effects of Common Chemicals. 2nd ed. Seattle: Healthy World, 2012. PDF.

(78) Mayo Clinic Staff. "Thalidomide: Research Advances in Cancer and Other Conditions." Mayo Foundation for Medical Education and Research, 18 Dec. 2010. Web. 04 June 2012.

(79) Miller MT, Strömland K. Teratogen update: thalidomide: a review, with a focus on ocular findings and new potential uses. Teratology. 1999 Nov; 60(5):306–321. 

(80) Medline Plus. "Thalidomide." U.S. National Library of Medicine, 11 Feb. 2012. Web. 04 June 2012.

(81) Gilbert, Steven. Children with Thalidomide-Related Birth Defects at a Swimming Pool. Digital image. Thalidomide., 30 Sept. 2011. Web. 04 June 2012.