Environmental Health Issues

41 Environmental Health Issues





The environment is a basic determinant of human health and illness. It is estimated that 13% to 37% of the global burden of disease can be attributed to three major categories of environmental risk factors: water, sanitation, and hygiene; indoor air quality; and outdoor air quality (Prüss-Üstün et al, 2008). Children between birth and 14 years old bear nearly half the burden of disease in low- and middle-income countries (World Health Organization [WHO], 2008). Environmental factors are estimated to contribute to 100% of lead poisoning, 30% of asthma, 5% of cancers, and about 10% of neurobehavioral disorders. In a classic study based on these estimates, the annual cost of environment-related illness in children in the U.S. in 2002 was calculated to be $54.9 billion (Landrigan et al, 2002). Since then, individual states have estimated costs that are at least as high or higher.


Chemicals, natural as well as synthetic, constitute a large part of the environmental risk to health, contaminating water, soil, and air. Naturally-occurring elements like radon cause lung cancer. There is sufficient scientific evidence of a causal link between prenatal or childhood exposure to methyl mercury, polychlorinated biphenyls, polychlorinated dibenzofurans, active maternal smoking (during pregnancy), environmental tobacco smoke (ETS) (during childhood), and 2,3,7,8-tetrachlorodibenzo-p-dioxin and adverse health outcomes in children and adults (Wigle et al, 2008). Research indicates that chemical exposure of the father or mother prior to conception, at the time of conception, and (for the mother and fetus) during pregnancy results in a gene-environment interaction that accounts for most adverse developmental outcomes of pregnancy (Mattison, 2010). Concern has been raised that human exposure to genetically modified organisms (GMOs) and to hormones fed to animals may contribute to cancers, hepatorenal toxicity, and long-term reproductive problems (de Vendômois et al, 2009). In 2009 the U.S. Department of Health and Human Services (USDHHS) and the Centers for Disease Control and Prevention (CDC) released the Fourth National Report on Human Exposures to Environmental Chemicals, showing that almost all subjects studied had measurable levels of many industrial toxins in their blood and urine (USDHHS and CDC, 2009). Yet despite the known effects of many environmental agents and despite the presence of toxins in almost all humans, a great deal of uncertainty about the relationship between the environment and disease and illness remains. Many providers are at a loss when confronted with questions about environmental health, do not know how to best approach it, or feel overwhelmed by the volume and complexity of environmental health information. The challenge lies in several areas:



Some providers may believe the effect of environmental agents is negligible, that lifestyle choices, genetic conditions, and/or infectious agents are responsible for most disease.


There is not always definitive evidence that exposure to an environmental agent causes a particular disease. Is the condition being seen clinically caused by environmental exposure or something else?


Exposure to some environmental agents may cause disease if there are preexisting or genetic conditions, or agents working together may cause problems (e.g., tobacco smoke and radon combined). It is often difficult for the provider to sort out the many variables.


Research findings vary as to the type of problem caused by an environmental agent. What effect does an environmental agent have on the human body? Using the Multiple Exposure-Multiple Effects model (Briggs, 2003), some agents can cause several problems, and many different agents may cause the same problem (e.g., cancer). Sometimes the effect may be so subtle as to be missed: a decline in IQ scores after exposure to lead may still leave the child within the range of “normal” IQ.


To what environmental agents has this individual been exposed? When? The health effect of an agent may be delayed for years and the exposure forgotten or unnoticed at the time it occurred (e.g., asbestosis, melanoma).


Some providers may believe that correcting environmental health problems is beyond their purview. Exposure to disease-causing agents, they think, is a systemic not an individual issue, so beyond treating the illness, they may feel they can do nothing to help their patients or change the system.


Providers feel inadequate to the task; they are not prepared well to manage environmental health concerns. Many providers state they lack knowledge and confidence in managing children’s environmental health issues, failing, for example, to know about and use available resources (e.g., the Pediatric Environmental Health Specialty Unit [PEHSU] in their region) (Trasande et al, 2010). Nursing and medical schools do not devote sufficient time to teaching about environmental health, and continuing education may be limited.


To complicate matters, this uncertainty on the part of providers and in the field of pediatric environmental health is taking place in a social and economic context where profit, not concern for health, drives corporate development. Companies that produce chemicals or GMOs often conduct their own safety testing, and the results may not need to be made public. Approximately 83,000 chemicals are registered for use in the U.S.; however, less than half of these have any laboratory testing at all. Almost 3000 of these chemicals are produced in quantities of 120 tons or more annually and 80% of these have no information available about developmental or pediatric toxicity. Further, the information available almost never considers interactions among chemicals or genetic susceptibility (Grandjean and Landrigan, 2006). Though corporations state they do not intend to cause health problems with their products, examples of environmental contamination, advertising to vulnerable groups (e.g., cigarettes to adolescents), cover-ups of harmful findings (e.g., tobacco company assertion that nicotine is not a health risk), and regulatory violations occur frequently (Shrader-Frechette, 2007).


Regulation of chemical toxins is difficult. The Toxic Substances Control Act (TSCA) of 1976 authorizes the U.S. Environmental Protection Agency (EPA) to require testing and reporting of some chemicals and to restrict mixing of some toxic substances. However, the requirements of regulation are high: the EPA must demonstrate that the chemical in question represents an “unreasonable risk” to human health in order to ban its use. Also, many chemicals used in cosmetics, foods, drugs, and pesticides are exempt from the law (Duderstadt, 2009).


Because it is difficult to establish direct cause and effect in the area of environmental health, it would be prudent to adopt a precautionary approach to environmental toxins. Many European nations operate using the precautionary principle, which stipulates that chemicals should not be introduced into the environment until they have been proven to be safe. In the U.S., unfortunately, a “cost-benefit” approach is used, in which the burden of proof falls on regulatory agencies (e.g., the EPA) to show that the chemical represents an “unreasonable risk” to health. The cost of testing and regulating chemicals to ensure they are safe is balanced against the health problems those chemicals might cause, and, to date, U.S. industry has successfully been able to argue that it can be “too costly” to control pollution and restrict exposure for many chemicals (Schapiro, 2007). As a result, many people are unnecessarily exposed. Health care providers across the U.S. must advocate for use of the precautionary principle to control exposure to environmental toxins nationally and internationally.


The current situation is grim, but it is important to note that health care providers are increasingly aware of the problem, and many efforts are being made to address environmental health in pediatric practices. A network of regional PEHSUs has been created to provide information, clinical consultation, and support for pediatric providers (see www.aoec.org/PEHSU.htm). In 1999, the American Academy of Pediatrics (AAP) published a pediatric environmental health manual for providers (Etzel and Balk, 2003). Educators are developing curricula and preparing materials for students in health disciplines (Beitz and de Castro, 2010; Jamil et al, 2010); some are suggesting a medical specialty in environmental medicine (le Moal and Reis, 2011), and tools for assessment and management of environmental variables continue to be written (Cohen Hubal et al, 2010; Judson et al, 2008; Kavlock and Dix, 2010). New technology allows for more sophisticated assessment of how chemicals affect the human body, and intricacies of the environment-health relationship are better understood. Lack of strong evidence for a cause-effect relationship is not due to absence of an effect; rather, more research is needed to clearly establish the connections (Wigle et al, 2008). In 2000, the U.S. Congress authorized the National Children’s Study to investigate the root causes of many childhood and adult diseases. It is proposed that 100,000 children be followed from before conception until 21 years old, examining environmental influences on health, including diet, ambient air, and home and school environments as well as interactions with various genetic traits. As of 2010, 37 regional participation sites had been identified; the challenge is to develop a recruitment plan, assessment tools, and protocols to coordinate, administer, and conduct the research (Savitz and Ness, 2010).


Health care providers need to be able to give their clients the most accurate information available about environmental health issues. Parents may suspect that an illness is associated with environmental conditions, or express concern about the risk of exposure to untested substances. The provider who is knowledgeable about the potential hazards of environmental exposure will be able to explain the possible connections, collect clear assessment data, and work closely with families to make appropriate treatment choices, including referral and consultation with public health authorities. If not personally knowledgeable, the provider should know where to get information. A core competency for all nurse practitioners (NPs) states that the NP “recognizes environmental health problems affecting patients and provides health protection interventions that promote healthy environments for individuals, families, and communities” (USDHHS, 2002). This chapter is designed to help prepare providers to meet this competency. In addition to direct patient care and education, primary health care providers can collaborate with other health care providers, conduct research to identify environmental problems, and advocate in the public arena (e.g., industry, policy, funding, and regulation) for more responsible management of environmental agents that affect health.



image Principles for Understanding Children’s Environmental Health



Children’s Increased Risk for Environment-Related Illness


Children, because of their developmental immaturity, rapid growth, size, and behavior, are particularly susceptible to environmental threats (Table 41-1). Exposure to toxins or other harmful substances affects growth and damages organs or body systems during critical developmental periods or windows of vulnerability, prenatally and during childhood. It is known, for instance, that a 50-mg dose of thalidomide, administered during the 26th day of gestation will likely result in major malformations to an embryo but that same dose taken at the 10th week of gestation will have no effects (Brent, 2004). Toxicants that cross the placenta (e.g., drugs, carbon monoxide [CO], mercury, lead, and cotinine [from environmental tobacco smoke]) can contribute to low birthweight, spontaneous abortion, intrauterine growth retardation, increased risk of cancer, poor cognitive and behavioral development, and birth defects. Approximately 3% of all babies born in the U.S. have a serious birth defect. The rate of some birth defects is increasing (Brent, 2004), and about 10% appear to be related to environmental exposure (Chervenak et al, 2010).



Children’s rapidly growing tissues more readily absorb environmental toxins; the lungs, skin, and gastrointestinal (GI) tract of newborns are highly permeable and gastric pH is high, facilitating absorption. At the same time, newborns’ immature organ systems more slowly metabolize drugs, making it more difficult for infants to detoxify and excrete harmful substances. Children consume more fresh fruit, water, milk, and juice per pound of body weight than adults; many of these products are treated with pesticides or other chemicals. Children engage in more outdoor activities than adults, breathe more pollutants per pound of body weight, and are physically closer to many potentially harmful substances. Crawling on floors, chewing on objects, and running and rolling in grass are behaviors that expose children to environmental toxins and can result in lead poisoning, pesticide poisoning, and respiratory problems, including asthma. Adolescents are particularly susceptible to environmental tobacco smoke and occupational hazards. Children living in poorer communities are at higher risk than others. Poor housing and nutrition, high levels of lead, toxic waste deposits, and limited access to health screening and treatment contribute to increased risk.


In addition to the immediate risk during childhood, children have a longer time span for exposure to environmental toxins, and with some conditions children are more likely to suffer health problems than adults exposed to the same substance.




Epidemiologic Model: Risk Assessment Approach


A first step in an epidemiologic approach (Fig. 41-1) identifies the interactive factors in the environment, including receptors (i.e., hosts or living things that are susceptible or exposed to environmental agents); toxins, or harmful substances that might cause damage (i.e., the agent); and the environmental medium, or route by which exposure could occur (e.g., air, water, or food).



A second step of risk assessment using an epidemiologic model is to determine the possibility that harm could occur. A number of questions are asked when making this determination:



A final step in this process compares the actual environmental condition with the applied action level, asking the following question: With the amount of exposure present, is the individual at risk for health problems?



Toxicologic Principles


Toxicologic principles are those the primary care provider has learned related to pharmacologic therapy: exposure, absorption, distribution, metabolism, tissue sensitivity, and effects—therapeutic or toxic. In fact, Paracelsus (1493-1541), considered the “father of toxicology,” is reputed to have said, “All substances are poisons; there is none that is not a poison. The right dose differentiates a poison from a remedy.”









image Primary Care Approach to Children’s Environmental Health



Assessment


Assessment of environmental health hazards should be integrated into regular health appraisals, as well as examinations of ill children. Figures 41-2, 41-3, and 41-4 list essential questions to ask for an environmental history, including questions related to asthma.








Management of Environmental Conditions


Management of illness related to environmental factors uses a public health model of primary, secondary, and tertiary prevention. A multidisciplinary approach that includes epidemiology, pediatrics, toxicology, public health, and health economics is necessary to treat specific conditions, as well as to prevent exposure to toxins. In addition to caring for acute exposures, providers should inform patients and families about health risks and the nature of environmental contaminants, advocate for healthy environments in the creation of public policy, and work with other professionals to report, monitor, and control exposures. The regional PEHSUs and many online sources provide information and support for clinical, toxicologic, educational, and policy work.



Primary Prevention


The goal of primary prevention is to keep a problem from occurring and to maintain a level of wellness. Education of individuals and the public to help them identify health hazards and prevent exposure is a form of primary prevention. Providers can find a wealth of information about specific toxins, patient support groups, advocate activities, and safety practices and regulations on the Internet. Primary prevention also includes assessment of communities and populations. Safety inspections in industry and public areas (e.g., school playgrounds); monitoring of lead or radon in homes, schools, and workplaces; and scientific research to determine connections between environmental agents and disease are examples of early assessment. It is important to conduct research on children, adapt research methodologies to the unique characteristics of children, and develop biologic markers to better assess the effect of environmental hazards on children as the National Children’s Study proposes to do.


Primary prevention also takes place at the public policy level. Regulations or legal restrictions can prevent health problems (e.g., through implementation of air and water quality standards, restaurant and food handling regulations, or bans on the use of hydrofluorocarbons). Various U.S. federal agencies function to regulate development and use of hazardous materials (e.g., the EPA, the U.S. Consumer Product Safety Commission, and the Occupational Safety and Health Administration [OSHA]). In 1997, the U.S. joined seven other countries (the G-8) in creating the 1997 Declaration of the Environment Leaders of the Eight on Children’s Environmental Health, raising the issue of protection of children from environmental threats to an international level (EPA, 1997).






image Common Environmental Agents and Adverse Effects


This section presents a brief discussion of general pediatric poisoning and some common environmental agents that are particularly hazardous to children.



General Pediatric Poisoning





Assessment (Rodgers et al, 2007)







Management


Management approaches for ingested poisons vary with the type of poison, amount of exposure, time lapse since exposure, and susceptibility of the child. Initial management focuses on airway, breathing, and circulation (the ABCs). No matter what poison was taken in, vital body functions must be maintained. Consultation with a poison control center is recommended.


If the patient is to be treated at home initially, the provider needs to talk with the parent or caregiver approximately ½, 1, and 3 hours after the ingestion. Changes in the child’s condition will dictate changes in the plan of care. If the child requires hospital care, an ambulance may be necessary and the emergency department personnel informed so that they can be prepared appropriately (Rodgers et al, 2007).


Subsequent management involves counteracting or neutralizing the effects of the poison (administration of antidotes), decreasing the amount of poison in the system (gastric decontamination), and providing life-support measures while the body detoxifies itself. For some poisons (e.g., warfarin), observation alone may be sufficient.


Basic decontamination guidelines for contact contaminants are listed in Box 41-1. Prompt action to remove the toxin from the skin (e.g. insecticide exposure) or from the eye may prevent major absorption. With ingested toxins, most liquid products are absorbed completely within 30 minutes and solids within 1 to 2 hours. Thus timing is critical, and because decontamination procedures also contain risks, one must consider whether the technique chosen is likely to be of sufficient value to merit its use. Activated charcoal, an adsorbent agent, has been demonstrated to have good efficacy for many, but not all, toxins. The toxins adhere to its surface, rather than being absorbed from the GI mucosa. The use of gastric lavage is coming into question more and more because it only removes a small portion of gastric contents. Syrup of ipecac is not recommended for use in poisoning (American Academy of Pediatrics [AAP], 2003; Rodgers et al, 2007). Cathartics are often used with activated charcoal but without good evidence to support use. Whole-bowel irrigation with a polyethylene glycol electrolyte into the stomach to cleanse the entire GI tract has been shown to be somewhat successful for substances that are absorbed slowly, such as iron or sustained-release medications (Rodgers et al, 2007).



Other strategies that can be used in the hospital setting include diuresis, dialysis, and hemoperfusion.





Lead



Description


Lead poisoning is the presence of blood lead levels (BLLs) that cause toxic effects on multiple organ systems. The major pathway of exposure is via ingestion although lead dust is absorbed through the lungs. Absorption depends on the route of exposure and the age and nutritional status of the individual (Agency for Toxic Substances and Disease Registry, 2010). One hundred percent of lead inhaled into the lower lungs is absorbed; in children, up to 70% of lead in the GI tract can be absorbed, in contrast to about 20% in adults. Once ingested, lead circulates through the body attached to erythrocytes. It affects heme production, competes with calcium for calcium-binding sites on proteins, and may affect any calcium-mediated process. It affects certain enzyme functions (e.g., ferrochelatase in bone marrow) and damages the nervous system, both through direct nerve cell damage and interference with nerve conduction. It also affects brain development as it inhibits the normal pruning process that eliminates multiple intercellular connections (Markowitz, 2007). Exposure to lead is linked with many conditions and diseases, including ADHD, reading problems, school failure, delinquent and criminal behavior, tooth decay, renal disease, and cardiovascular disease (Froehlich et al, 2009; Lanphear et al, 2005; Wright et al, 2008). Prenatal lead exposure has been associated with schizophrenia (Opler et al, 2008).


Children and adults differ in lead exposure sources, absorption, metabolism, and specific ways in which toxicities are expressed. Children are more likely to be exposed via hand-to-mouth behaviors; the fraction of lead absorbed from the gut is higher in infants and children, and the amount absorbed increases in children when nutritional deficiencies, such as iron and calcium, are present. Temporary peripheral neuropathies from lead toxicities predominate in adults, whereas permanent central nervous system effects predominate in children. If children have higher BLLs at age 6 years than they did at age 2 years, they are more likely to have IQ deficits and behavior problems than children who have a higher BLL at age 2 than at age 6 (Hornung et al, 2009).


Over the past 30 years, the definition of the BLL considered to be toxic has been revised downward. The toxic level for clinical assessment in the U.S. is 10 mcg/dL or more, but even at lower levels, impairment of cognitive function occurs. Studies show clear, persistent intellectual impairments at levels of less than 7.5 mcg/dL (Lanphear et al, 2005). Some experts are calling for a toxic level of 2 mcg/dL, recognizing that no level is totally safe (Gilbert and Weiss, 2006; Wigle et al, 2008).



Epidemiology


Although environmental lead sources have decreased in the U.S., lead poisoning continues to be a serious environmental health problem for young children. Approximately 1% of children tested in 2007 had elevated BLLs, and it is estimated that more than 310,000 children 1 to 5 years old in the U.S. have lead levels above 10 mcg/dL (Warniment et al, 2010). A recent study of more than 200,000 children found a positive association between poverty and pre-1950s housing and lead toxicity, with 17.3% of the children having BLLs greater than 10 mcg/dL (Vivier et al, 2010). Boys may be more susceptible than girls to the effects of prenatal exposure to low levels of lead (Jedrychowski et al, 2009).


The major source of lead poisoning in children is dust and chips from deteriorating paint on interior surfaces. Before 1950, much white house paint was 50% lead and 50% linseed oil. Limits on the lead content of paint began in 1955 and were augmented in 1971 and 1977. The prevalence of lead hazards in homes built before 1960 is five to eight times greater than in homes built between 1960 and 1977, and 14 to 23 times greater than in homes built between 1978 and 1998 (Jacobs et al, 2002). Children are at greatest risk in houses where paint is peeling or those where renovation with paint removal is occurring. Lead dust is more readily absorbed than chips. Soil near deteriorating homes, mines, lead-using industries, and smelters can have high lead levels. Acidic water with low mineral content can leach lead from lead pipes or solder. Hot water leaches more lead than cold. Brass fixtures also contain lead. Food can be a source of lead. For example, lead from soil can contaminate root vegetables. Some other sources of lead are listed in Table 41-2. Lead crosses the placenta so that the fetal and newborn blood level is close to that of the mother’s, but little lead is transferred in breast milk.


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Jul 24, 2016 | Posted by in PEDIATRICS | Comments Off on Environmental Health Issues

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