In all areas, EPA is interested in research that recognizes issues relating to environmental justice, the concept of achieving equal protection from environmental and health hazards for all people without regard to race, economic status, or culture. Over the past few years, public attention has increasingly focused on potential adverse health effects in children from exposure to toxic chemicals in their food, water, or environment.
Public health officials and physicians are being asked to assess the significance of a plethora of possible risks for children. At the Federal level, recent actions by the President, the Congress, and the EPA Administrator have focused attention on environmental health threats to children.
In , President Clinton issued an Executive Order addressing protection of children from environmental health risks. The Food Quality Protection Act of and the Safe Drinking Water Act of both require consideration of infants and children in risk assessments used to determine acceptable levels of environmental contaminants in food and drinking water.
In , EPA Administrator Browner issued a report entitled Environmental Health Threats to Children and set a Children's Agenda for EPA, calling for consideration of children's risks in all Agency actions and a greater emphasis on research to support children's risk assessments. The health impacts of most concern are respiratory diseases, childhood cancer, immune system effects, neurotoxicity, and developmental effects. From to , the prevalence, morbidity, and age-adjusted mortality rates for asthma increased significantly despite improvements in asthma diagnosis and management and improved understanding of the biology and immunology of the disease.
There are a limited number of studies that suggest age-related differences in cancer susceptibility. However, it is still difficult to assess the potential impact of these differences due to a lack of research.
The immune system is of concern due to the known differences in immune structure and function between children and adults. Exposure to some toxic chemicals, such as lead, are well known to cause neurological effects in children. However, the potential neurological effects of other metals and chemicals such as solvents and pesticides are not as well understood.
Finally, exposure to a variety of toxic chemicals in the environment can affect initial growth and development.
In addition, exposure during crucial periods of development may have profound effects which may or may not be reversible in later life. These, among other concerns, support the need for additional research on possible environmental causes of childhood diseases. In exploring the factors that affect health risk from exposure to toxic chemicals, it must be remembered that children are a unique sub-population. Depending on the circumstances, children may be more or less susceptible to the toxic effects of these chemicals than are adults.
Risks to children may differ qualitatively or quantitatively from risks to adults because of differences in their immature physiology, metabolic processes, respiratory rates, and differing levels of exposure. Nutritional status, disease, and genetic variation can affect many of these processes, increasing or decreasing the risk from exposure to toxic substances.
In response to this RFA the EPA will sponsor research to better understand how these factors affect risk to children from exposure to toxic chemicals in the environment. Of particular interest are pesticides such as pyrethroids and the triazine herbicides. Projects which explore the assessment of intermittent and time-varied exposures as well as the biological basis for increased susceptibility among children will be particularly valuable.
Proposals focusing exclusively on lead poisoning in children will be considered non-responsive to this RFA. The exposure of children to potentially toxic chemicals is generally quite different from that to adults because of differences in physical environment, activity patterns, and diet.
The assessment of exposure in children and adults depends on first being able to consider all relevant exposure pathways, including dietary, drinking water, respiratory, dermal, and non-dietary oral ingestion.
Exposures that occur via some of these pathways may be relatively high, but are usually not persistent and often result from human activities that are relatively rare or intermittent. Many of the differences in exposure between children and adults are associated with these types of exposure and are most often linked with the unique behavior of children. Therefore, it is important that we better understand the temporal variation in the environmental and behavioral factors that influence exposure.
Children's daily activities, proximity to floors, carpets, lawns, and soils, the frequency and duration of hand to mouth behaviors, and many other factors combine to form a life environment that varies with age and from child to child.
Body fat, on the contrary, increases rapidly up to 6 months and then decreases, accounting for similar percentages of body weight at ages 4 and 12 months [ 5 ].
Metabolism and elimination rates are generally lower in neonates than in adults. Many metabolic pathways are not fully developed in the infant. Renal clearance is lower in neonates than in older children and adults for all classes of chemicals.
The maturation of these metabolic and elimination rates can result in the mobilization of chemicals, and higher exposures of the target organs or systems to the products of metabolism. In terms of excretion, certain life stages such as pregnancy, lactation, and also menopause, will result in the mobilization of chemicals from fat or bone stores, and the exposure of other organs or the developing fetus and lactating child to the toxicants that were accumulated in the mother.
From conception to birth, the human organism advances rapidly through a complex set of developmental processes that culminate in the newborn. These development processes include cell division, organ formation, and growth as well and functional development. During development, some biological processes occur only during certain stages of development and not in others, or they occur at a different rate in different developmental stages.
For example, cell division in most organs takes place rapidly during early development and much more slowly at later stages. Other processes such as apoptosis, or programmed cell death, occur more widely during development and are less prominent during adulthood. These biological processes need to be effectively coordinated and require the cellular and intercellular signaling systems to work correctly.
Because of the complexity and speed at which these processes take place and the intricate relation between them, interference at the sequence of any of these processes can have damaging and irreversible effects.
Exposure to environmental toxicants can have a completely different effect depending on whether it occurs at one developmental stage or another. In addition, damage due to environmental exposures may occur and manifest itself immediately, or may not appear until subsequent stages of development, after development is complete, including late adulthood. The following sections describe the current state of knowledge about the windows of susceptibility during childhood development.
Germ cells sperm and egg cells carry the genetic information from each parent that will provide the unique genetic blueprint for each child. In the male fetus, primordial germ cells develop in utero. From puberty to adulthood, these cells undergo cell division, mitosis, and meiosis, to produce mature sperm and continue to be produced from stem cells through adulthood.
In females, primordial germ cells undergo mitosis and the first phase of meiosis during fetal life, and in women, mature oocytes are produced every month from follicular cells. In animal models, preconceptional carcinogenesis has been demonstrated for a variety of types of radiation and chemicals, with demonstrated sensitivity for all stages from fetal gonocytes to postmeiotic germ cells [ 11 ]. Results of environmental damage to germ cells may include reduced fertility later in life or offspring with congenital health problems [ 12 , 13 ].
For example, men exposed to diethylstilbestrol DES in utero had lowered sperm count and increased frequency of abnormal sperm [ 14 ].
There is a substantial body of evidence demonstrating that exposures to environmental agents and medical radiation can injure germ cells in such a way as to cause increased incidence of cancer, particularly leukemia, among offspring of the exposed individuals.
For example, paternal exposures to benzene have been linked to leukemia and lymphoma in children [ 15 ]. Animal studies support these findings [ 11 ]. Several stages of embryonic and fetal development are susceptible to environmental harm. This high level of metabolic activity provides for a wide range of opportunities for environmental agents to interfere with cell development and growth.
Environmental toxicants may interact directly with DNA e. A toxicant that interferes with gene expression may prevent the synthesis of enzymes necessary for toxicant metabolism, resulting in the accumulation of the toxicant in the body.
DNA activation by a chemical may result in excessive synthesis of enzymes that catalyze the bioactivation of a toxicant production of a toxicant metabolite more toxic than the compound originally present. Chemicals can interfere with the activation or inactivation of genes that occur during early fetal life and that may be essential for the protection of the organism to external or internal harmful processes. For example, interference with genes involved in DNA repair, such as p53, a tumor suppressor gene important for DNA repair, may result in enhanced vulnerability to specific toxicants during development.
Studies with transgenic mice that are missing this gene have shown an increased sensitivity of mice fetuses to benzo[a]pyrene exposure and an increased death rate when exposed to the chemical during gestation [ 16 ]. Damage to p53 in humans could likewise increase sensitivity to agents that damage genetic material.
If a toxicant interferes with cell differentiation, cells may not reach their specific form and function necessary for their final role in the body, and organ function may be compromised.
Also, undifferentiated cells may be more vulnerable than differentiated cells to toxic effects. Some chemicals such as ethanol [ 17 ] and TCDD [ 18 ] have been demonstrated to affect specific types of undifferentiated cells.
Apoptosis or programmed cell death is a critical biological process for healthy development. Apoptosis involves the removal of certain cell types when they are no longer necessary. In some instances, one type of cell is succeeded by another during a specific developmental period. Apoptosis is involved, for example, in the elimination of cells in the immune system that, if they survived, could cause autoimmune disease [ 19 ]. Apoptosis is also critical in the development of the nervous system, where phases of cell proliferation alternate with phases of apoptosis on the basis of the progression of neuronal development [ 20 ] and remains active through the postnatal period because of ongoing nervous system development.
Normal patterns of apoptosis may be altered through altered gene expression or failure of signaling mechanisms resulting from environmental exposures. Certain autoimmune lympho-proliferative diseases and certain cancers have been related to the disruption of normal patterns of apoptosis. Neuronal migration is an important process in nervous system development and its alteration may result in irreversible damage.
For example, schizophrenia is thought to result, in part, from abnormal neuronal migration [ 22 ], but the role of prenatal exposures to environmental agents in causing this disease is not clear.
Exposures to ionizing radiation and methylmercury, for example, have been shown to affect the migration of neurons during development [ 20 , 23 ]. During the period of organ development, which occurs varying according to organ system between the 3rd and 16th week, disruption of development can disrupt the large-scale structure of organs, often resulting in physical malformations congenital anomalies.
The best known example of such gestational damage is exposure to diethylstilbestrol DES. DES caused genital anomalies among male children born of women who took the medication before the 11th week of gestation twice as often as among those who were exposed later in gestation [ 14 ]. Other effects such as low birth weight, pregnancy complications, or late fetal death have been shown to be a result of environmental exposures during later stages of prenatal development [ 24 ].
Disinfection by-products have been linked to the risk of spontaneous abortion for some time. There is now fairly consistent evidence for associations between early and late fetal deaths and indices of transplacental exposure to disinfection by-products [ 25 — 27 ]. Maternal smoking during pregnancy increases the risk of pregnancy loss, stillbirth, and infant mortality [ 28 ].
Several organs and systems continue to grow and develop during childhood and in some cases almost until adulthood.
For example, neuron migration, cell proliferation, and synapse formation are very active until 3 years of age, and myelination continues until adolescence [ 29 ] and possibly well into adulthood [ 20 ].
The immune response is also immature at birth and develops during infancy and childhood until about 1 year of age, while establishment of immunologic memory is not fully established until 18 years of age [ 30 ]. Exposure to environmental agents during early childhood may affect immune system development and may contribute to the development of certain diseases such as asthma and cancer later in life. Physical growth and maturation of organ systems continues through adolescence.
The process of sexual maturation is accompanied by complex interactions between the central nervous system and hormone-secreting organs, which can be affected by environmental exposures.
For example, the risk of breast cancer has been found to be greater among women who were exposed to radiation before 20 years of age [ 31 ]. Many important metabolic and biotransformation processes are poorly developed in the fetus, and full metabolic activity is not fully developed until after childbirth. Metabolism can increase or decrease the toxicity of a chemical, depending on the metabolic products of the chemical and pathway involved.
Metabolism may also make elimination from the body easier or harder, although the most common metabolic pathways usually render chemicals more hydrophilic and thus, more easily excreted.
In some cases, the adult biotransformation of a certain chemical may consist of a bioactivation pathway that makes the compound more hazardous than the one originally present. The absence of a metabolic pathway may result in the bioaccumulation of the chemical in the body and a later bioavailability and disposition to exert its toxic effects.
Immaturity could be an advantage if the activation pathway is not present in the fetus or child and there is an alternate pathway for the toxicant to be metabolized.
However, according to [ 32 ], given the primary evolutionary function of detoxifying and eliminating potentially toxic chemicals, immature or underdeveloped metabolic pathways are likely to render infants and children more sensitive to common environmental contaminants. Heavy metals are natural elements that have been extracted from the earth and used in human industry and products for centuries.
As a consequence of human activity, concentrations of heavy metals in air, water, and surface soil today are hundreds of times higher than in the preindustrial era. Some metals are naturally found in the body and are essential to the functioning of critical enzyme systems. Iron, for example, prevents anemia, and zinc is a cofactor in over enzyme reactions. Magnesium and copper are other familiar metals that, in minute amounts, are necessary for proper metabolism to occur.
The body has need for approximately 70 trace elements, but there are others, such as lead, mercury, aluminum, arsenic, cadmium, and nickel, that have no roles in human physiology and can be toxic at even trace levels of exposure. Nutritionally, heavy metals can compete with nutrient elements, such as the case of lead, which is stored in the bones in the place of calcium.
Metals are notable for their wide environmental dispersion, their tendency to accumulate in select tissues, and their overall potential to be toxic at even relatively minor levels of exposure. In general, heavy metals are systemic toxins with specific neurotoxic , nephrotoxic , fetotoxic , and teratogenic effects. Heavy metals can directly influence behavior by impairing mental and neurological function, influencing neurotransmitter production and utilization, and altering numerous metabolic body processes.
Exposure to heavy metals can occur through drinking water, air, or ingestion of heavy metal—contaminated soil. The amount that is actually absorbed from the digestive tract can vary widely, depending on the chemical form of the metal and the age and nutritional status of the individual.
Once a metal is absorbed, it distributes in tissues and organs. Excretion of metals typically occurs through the kidneys and digestive tract, but they tend to persist in some storage sites, like the liver, bones, and kidneys, for years or decades.
Lead is one of the best known heavy metals in terms of its toxicity. During pregnancy, body stores of lead may be mobilized and transferred from the mother to the fetus [ 33 ]. Behavioral characteristics of children later on, such as the hand-to-mouth behavioral pattern of 1—3 year olds, can result in high exposure and internal levels of lead. Lead paint is a major source of environmental exposure for children who ingest flaking paint, paint chips, and weathered powdered paint mostly from deteriorated housing units in urban areas.
Lead can leach into drinking water from lead-based solder used in water pipes. Lead also leaches into foods or liquids stored in ceramic containers made with lead glazing, which is still used in some countries.
The absorption of lead from ingestion of lead-contaminated water is higher for children than for adults, so that for a given level of exposure, the resultant internal dose is higher in children than in adults [ 3 ]. Children are also more sensitive than adults to the toxicological effects of lead at a given internal exposure level.
The lowest observed adverse effect levels LOAELs for several health endpoints occur at lower blood lead levels in children than in adults. The most sensitive targets for lead toxicity are the developing nervous system, the hematological and cardiovascular systems, and the kidney. Mercury is a ubiquitous heavy metal of both natural and anthropogenic sources. Mercury occurs in both inorganic and organic forms, and it is most hazardous in its organic form of methylmercury. The nervous system is very sensitive to all forms of mercury.
Methylmercury and metallic mercury vapors are more harmful than other forms, because methylmercury can cross the blood brain barrier. Methylmercury in the marine and freshwater environment is absorbed by fish and shellfish and bioaccumulates in the food chain. Increased risk is of particular concern in children and in populations that have an increased dietary exposure to fish. Arsenic occurs naturally in the environment and in some areas of the world is a natural contaminant of underground water that is used as drinking water.
It is also an anthropogenic contaminant. Once absorbed into the body, arsenic undergoes some accumulation in soft tissue organs such as the liver, spleen, kidneys, and lungs, but the major long-term storage site for arsenic is keratin-rich tissues, such as skin, hair, and nails.
Cadmium is another chemical that is toxic to adults, although it has not been extensively studied in children. The US Department of Health and Human Services has determined that cadmium and cadmium compounds are known human carcinogens.
Cadmium has been linked to diminished kidney function lung disease, chronic bronchitis, and lung, kidney, and prostate cancers. In the USA, smoking is the primary source of cadmium exposure, although high levels of cadmium can also be found in organ meats, shellfish, and vegetables. Pesticides are substances that are used to prevent, repel, or destroy pests — organisms that compete for food supply, adversely affect comfort, or endanger human health FIFRA More than 20, pesticide products with nearly active ingredients are registered for use as insecticides, miticides, fumigants, wood preservatives, and plant growth regulators.
It cannot be denied that pesticides have beneficial economic and also public health impacts. Pesticide usage helps improve human nutrition through greater availability, longer storage life, and lower costs of food. It also reduces human labor requirements and attendant risks of injury.
Pesticides also assist in the control of food-borne and vector-borne diseases, such as malaria, which kill millions of persons in the world. Pesticides also pose human health concerns because they are toxic substances and widely spread in the environment.
Although the toxic mechanisms on targeted pest species are well characterized, the potential for adverse health effects in humans is not fully known.
Pesticides are composed of several classes of chemicals with different mechanisms of action. Most insecticides work by interfering with nervous system function. Organophosphates, which account for approximately one-half of the insecticides used in the USA, and carbamates, which are widely used in homes and gardens, inhibit the activity of acetyl cholinesterase at nerve endings, resulting in an excess of acetylcholine in the synapsis and a depolarizing blockage of neural transmission.
The effects of carbamates are readily reversible and of shorter duration. Organochlorines, such as dichlorodiphenyltrichloroethane DDT and lindane, interfere with nerve cell membrane cation transport, resulting in neural irritability and excitation of the central nervous system.
Herbicides, including the chlorophenoxy compounds 2,4 D and 2,4,5 T are primarily irritative to the skin and respiratory tract during acute exposures and work by different mechanisms. Some substances, such as paraquat, are highly corrosive and can cause multisystem injury and progressive pulmonary failure [ 34 ].
Arsenical pesticides, such as copper chromium arsenate, have been used, until recently, as wood preservatives to prolong the useful life of exterior wooden structures. These compounds cause central nervous system depression at sufficient doses. Pesticides are ubiquitous in the environment. They are found in food, water, homes, schools, workplaces, lawns, and gardens.
They are present in soils that have been spread with pesticides or where pesticides from adjacent agricultural areas have drifted, and may reach water supplies from agricultural runoff. In the USA alone, more than 0. In developing countries, many highly toxic and biologically persistent pesticides such as parathion, DDT, and paraquat, which are no longer permitted in many developed countries, are still in wide use and result in chronic exposures and acute, too often fatal poisonings of thousands of young children each year.
Most children in the world are exposed to some degree to pesticides. Children in rural and agricultural areas and especially children whose parents are farmworkers or pesticide applicators are at highest risk of having increased exposures to pesticides. Pesticides may reach their homes due to the drifting of pesticides that are applied to the ground through aerial spraying.
Children may work or play near their parents in the fields where pesticides have been used. Parents who work with pesticides may bring pesticides to their homes, impregnated in their clothes and bodies. In countries where residential housing with gardens and lawn predominate, homes and garden pesticide use may result in significant levels of exposure [ 34 ]. Exposure of children to pesticides may occur through inhalation, ingestion, and dermal absorption.
Ingestion of pesticides occurs either through accidental exposure due to pesticides stored in food containers i. Foods grown in pesticide-contaminated soils and fish from pesticide-contaminated water can also carry significant amounts of pesticides. Children may also ingest pesticides adhered to the surface of toys or other objects through their hand-to-mouth behavior.
The potential of dermal exposure of children to pesticides is higher than that of adults because of their relatively large body surface area and extensive contact with lawns, gardens, and floors by crawling and playing on the ground. Prenatal and early childhood exposures are of special concern because of the susceptibility of the developing organ systems to pesticides the central nervous system in particular as well as behavioral, physiological, and dietary characteristics of children.
Breast-feeding infants may ingest pesticides or pesticide metabolites present in the breast milk. The quantity of pesticide that is passed to the infant via breast milk is influenced by many variables such as maternal age and parity, maternal body burden of the chemical, and breast-feeding patterns. As infants are weaned and progress to solid foods, they consume, per unit of body weight, proportionally more fruit and more fruit juice than adults.
Environmental tobacco smoke ETS , also known as second-hand smoke, is exhaled smoke and sidestream smoke emitted from the burning of the tip of the cigarette. The effects of passive smoking begin in utero, where constituents of tobacco smoke, such as PAHs, nicotine, and carbon monoxide, cross the placenta and are concentrated in the fetal circulation [ 35 ].
Children are also exposed during childhood if any of the parents smoke. Polychlorinated biphenyls are synthetic compounds with two linked phenyl rings and variable degrees of chlorination. They have been used for many years because of their thermal and chemical stability. They are nonvolatile, hydrophobic oils that are not easily biotransformed in the environment or metabolized by the human organism, so they are very persistent in the environment, and bioaccumulate in the food chain and in the fat compartment of the human body.
Although they have been banned in the USA for more than 30 years, they are still widely present in the environment. They have been found in wildlife, human tissue, and human milk.
Polychlorinated dibenzodioxins PCDDs , commonly referred as dioxins, are formed during paper bleaching and waste incineration.
One dioxin congener, 2,3,7,8-tetrachlorodibenzo-p-dioxin TCDD , is considered to be the most toxic synthetic chemical known. The most significant source of exposure is contaminated food, particularly fish at the top of their trophic chain.
Of greatest concern are the populations that consume high amounts of fish. Because PCBs and PCDFs are not metabolized or excreted, they can accumulate in the fat tissue of the body, as well as in human milk, resulting in high exposures of the developing fetus and the newborn.
Disinfection by-products DBPs form when disinfectants are added to drinking water and react with naturally occurring organic matter. Chlorine, the most widely used primary disinfectant, reacts with naturally occurring organic matter to form a range of unwanted by-products such as the trihalomethanes THMs which include chloroform, bromodichloromethane BDCM , chlorodibromomethane DBCM , and the haloacetic acids HAAs , such as monochloroacetate, dichloroacetate, and trichloroacetate. Exposure to DBPs occurs through ingestion of water or through inhalation and absorption during showering, bathing, and swimming.
While there is some concern that these chemicals may pose a health risk, the potential risks arising from not treating drinking water are considerably greater, and the disinfection of water should never be compromised as a result. The developing nervous system is more susceptible than the adult brain to the disrupting effect of toxic chemicals [ 5 ]. The lengthy period of brain development and the extensive number of processes needed to take place contribute to the susceptibility of the developing nervous system.
In the 9 months of pregnancy, the human brain and spinal cord must develop from a thin strip of cells along the back of the embryo into a complex organ comprised of billions of precisely located, highly interconnected, and specialized cells. Brain development requires that neurons move along precise pathways from their points of origin to their assigned location, that they establish connections with other cells near and distant, and that they learn to intercommunicate.
Each connection between and among neurons must be precisely established at a particular point in development, and redundant connections need to be pruned away through programmed cell death, apoptosis. All these processes must take place within a tightly controlled time frame, in which each developmental state must be reached on schedule and in the correct sequence. Critical windows of vulnerability, which exist only in the 9 months of pregnancy and to a lesser extent in early childhood, are unique to early brain development.
They have no counterpart in adult life. Exposure to toxic chemicals during these windows of vulnerability can cause devastating damage to the brain and nervous system. Any toxic or other environmental exposure that interferes with the tightly orchestrated sequence of events involved in brain formation is likely to have profound effects on intellect, behavior, and other functions.
If a developmental process in the brain is halted or inhibited, if cells fail to migrate the proper sequence to their assigned locations, if synapses fail to form, or if pathways are not established, there is only limited potential for late repair, and the consequences can be permanent [ 36 ].
Environmental toxicants can affect both the structural and functional development of the nervous system. Depending on the developmental stage at which exposure occurs, sensory development, intelligence, or behavior will be affected differentially. While early-developing neural systems have been considered the most vulnerable to chemical insult, scientists have called attention to the importance of chemical exposure that occurs late in childhood, as it has been recently suggested that behavioral and physiological foundations of cognition continue to develop during childhood and adolescence [ 5 , 37 ].
Exposure to environmental toxicants such as lead, methylmercury, and certain pesticides and PCBs even at very low levels have been shown to produce neurobehavioral functional deficits, and increased susceptibility to neurodegenerative diseases much later in life [ 38 ]. Of critical concern is the possibility that developmental exposure to neurotoxicants may result in an acceleration of age-related decline in function that could lead to Parkinson Disease, Alzheimer Disease, and other forms of brain degeneration.
This concern is compounded by the fact that developmental neurotoxicity that results in small effects on the individual at a particular stage can have a profound societal impact when considered in the whole population or across the life span of the individual [ 36 ]. Behavior is also disrupted, sometimes permanently, by such exposures. The following sections will give a short overview of some neurotoxicological effects of the best known chemicals for their effect on the developing nervous system.
Some toxicants such as ethanol have been excluded, as the focus of this chapter is on exposures to toxicants to which the majority of children are exposed. Lead is one of the best studied toxicants and one of the few pollutants for which susceptibility of children has been clearly established.
The best known health effects on children are its neuropsychological effects although other effects have also been studied and are partially documented. The neurotoxic effects of lead in children have been extensively studied.
One distinctive characteristic of the research findings on lead neurotoxicity over the past 2—3 decades is that it has led to a progressive decline in the LOAELs lowest observed adverse effect levels. The early finding in the s by Landrigan et al. However, epidemiological studies during the last decade have found strong evidence for cognitive deficits among school-aged children at blood lead levels below the current CDC action level [ 41 , 42 ].
Research has also demonstrated a link between developmental lead exposure and behavioral outcome. In a prospective study, the behavior of lead-exposed children at 8 years of age was significantly related to tooth dentine levels [ 44 ], suggesting that social and emotional difficulties correlate with lead exposure.
In another prospective, longitudinal study, both prenatal and postnatal lead exposure was related to antisocial and delinquent behavior in adolescents [ 45 ]. It is generally accepted in the scientific and medical community that the adverse neurobehavioral consequences of lead are not reversible and remain in place across the life span [ 41 ].
Further, the possibility that a threshold level for the effects of lead does not exist has been suggested [ 42 ]. Methylmercury is a well-established neurotoxicant that can cause serious adverse effects on the development and functioning of the human central nervous system, especially when exposure occurs prenatally.
The well-known episodes of community-wide poisoning in Japan and Iraq revealed the particular sensitivity of the fetus to the toxic effects from mercury exposure. In these communities, pregnant women exposed to methylmercury and who themselves had no or minimal symptoms, had babies with devastating neurological handicaps, including delayed attainment of developmental milestones, blindness, deafness, and cerebral palsy.
At levels of exposure lower than those encountered in the Minamata Bay, there is limited epidemiological evidence of neuropsychological effects. A birth cohort of 1, children was established at the Faroe Islands in —, and the methylmercury exposure was determined from the mercury concentration in the cord blood [ 46 ]. Neuropsychological effects in the areas of language, attention, and memory and to a lesser extent in visuospatial and motor functions were observed [ 46 ].
In Brazil, cross-sectional studies of Amazonian children aged 7—12 years show mercury-associated effects in agreement with the Faroe findings [ 47 ]. However, a large cohort study conducted in the Seychelles did not reveal consistent associations between perinatal methylmercury exposure indices and developmental milestones or neuropsychologic test scores up to age 5 years old [ 48 ]. These findings are supported by animal studies, showing that transplacental or postnatal methylmercury exposure affects auditory systems at the cortical level [ 50 ].
The important question is to which degree these findings relate to fish-consuming populations in general. Although this question cannot be answered with any confidence at this time, it looks like the recommended one to two fish meals per week during pregnancy would be very unlikely to cause any risk to the fetus, unless the seafood is severely contaminated.
The National Academy of Sciences recommended that a limit of about 0. Polychlorinated biphenyls are known to interfere with thyroid hormones, some of which are critical for normal brain development, and this effect of PCBs on the thyroid function of the newborn has been postulated as the mechanism of action of neuropsychological effects [ 52 ]. The earliest evidence of PCB-related neurotoxicity comes from the poisoning episodes in Japan Yusho and Taiwan Yucheng where people became ill after ingesting rice oil that was highly contaminated with PCBs.
Infants born to mothers who consumed PCB-contaminated rice oil during pregnancy were at increased risk for low birth weight, abnormal brown pigmentation of the skin, and clinical abnormalities of the gingival, skin, nails, teeth, and lungs [ 53 ].
In addition, children of both cohorts had various neurobehavioral deficits such as delayed attainment of developmental milestones, lower scores on intelligence tests, and higher activity levels [ 54 ]. Children were followed and examined 6 years later and showed persistent behavioral abnormalities and ectodermal defects [ 55 ]. 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.
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.
Heavy metals are elements with high atomic masses. Heavy metals with no known benefit for human physiology are considered "toxic metals" and include lead, mercury, and cadmium. Other heavy metals are necessary for life, including zinc, cobalt found in vitamin B , and iron found in hemoglobin.
Furthermore, trace elements, such as copper, manganese, selenium, chromium, and molybdenum, are important to the human diet. While it is well known for its use as a poison, arsenic is also used in wood preservatives, pesticides, and semiconductors. Background exposure to arsenic in air is typically less than 0. Studies in the s found that inorganic arsenic is a human carcinogen; since the U.
Safe Drinking Water Act of , nearly all pesticides based in inorganic arsenic compounds have been banned or voluntarily removed from the market. High and prolonged workplace exposure to inhaled arsenic has been associated with an increase in lung cancer, and some studies have suggested that workplace exposure to arsenic may increase the risk of skin, stomach, and kidney cancers, as well as leukemias and lymphomas. 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 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. 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.
Studies of people with high levels of arsenic in drinking water in Southeast Asia and South America have found higher risks of bladder, kidney, lung, skin, colon, prostate, and liver cancer. Arsenic poisoning in drinking water in Bangladesh and West Bengal, India, is considered by some to be the worst mass poisoning in history.
As a result, around 75 million people in affected regions of Bangladesh and India have been exposed to arsenic-contaminated water, and , to , deaths due to arsenic-induced cancer are expected in the future. Furthermore, exactly how arsenic leaches into the water is not clear, making the problem 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, India and Bangladesh or to let water sit out for a while so that inorganic arsenic can be converted into less harmful organic arsenic. In fact, federal and state regulatory standards have reduced the amount of lead in the air, drinking water, soil, consumer products, food, and in workplaces.
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 who suffering from lead poisoning are exposed to lead at work, especially in occupations related to welding, renovating, manufacturing car batteries, and maintaining bridges and water towers. Children are most vulnerable to lead poisoning. In fact, two-year olds exposed to lead have the highest blood level concentration of lead, partly because they place many objects and toys, some laden with lead, in their mouths.
When the city of Flint, Michigan, under state-appointed emergency management, changed its water supply from Lake Huron to the Flint River in , residents almost immediately began to complain about changes in color, taste, and odor. The water from the Flint River was highly corrosive and when it traveled through lead pipes to reach the residents of Flint, the lead concentration in the drinking water began to rise.
Elemental mercury is found naturally as an odorless, shiny liquid metal. 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. 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.
Organic mercury, or mercury covalently bound to carbon, impairs neurological development in fetuses, infants, and children, because methylmercury can pass from mother to fetus through the placenta.
Inorganic mercury, or mercury bound to inorganic compounds, often causes skin rashes, inflammation, muscle weakness, mental disturbances such as mood swings and memory loss, impairment of coordinated movements, and numbness in hands, feet, and sometimes the mouth. Many people are concerned with mercury levels in fish. Soon after, the EPA confirmed that more than 1. The EPA and FDA recommendations targeted pregnant women because fetuses are especially vulnerable to mercury poisoning.
Some fish contain dangerous levels of mercury for all people.
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