Pediatricians now treat many childhood health problems that are caused or exacerbated by environmental factors. In fact, nearly all pediatricians report a past experience with a patient who was affected by an unhealthy exposure.1 The World Health Organization (WHO) reports that more than 3 million children worldwide die each year due to environment-related causes.2 The rapid physiological development during the pre- and postnatal period leaves children highly susceptible to the effects of deleterious environmental exposures. Exposures during critical windows of development likely have a cascading effect that can influence health and well-being throughout a child’s lifetime. Environmental influences also contribute to the health disparities among communities of color in our country.
Most pediatricians want to know and to do more to reduce harmful environmental exposures and to strengthen protective factors among their patients.1 Most pediatricians are knowledgeable about the mechanisms through which the environment affects the health of their patients3 and can help families prevent or better manage conditions associated with environmental exposures.
As trusted sources of information by parents and within the community,3 pediatricians can also play an important role in the formulation of and advocacy for policies relating to environmental conditions. In the US, difficult policy debates, such as those relating to pollution regulation and smoke-free ordinances, have turned on the availability of compelling evidence and testimony from physicians.
In this article, we review the effects of environmental exposures from three natural resources (water, land, and air) with the potential to cause widespread negative effects on child health, and one environmentally mediated disease — asthma. We discuss the ways in which pediatricians can address these exposures in day-to-day clinical practice, and consider how pediatricians can act individually and through professional and advocacy groups to influence environmental policy affecting childhood health outcomes.
Exposure to Methylmercury
Clean water is central to the health of all children. Contaminants with potential effect on child health are present in surface and ground water, and originate from manufacturing industries, municipal sewage treatment plants, overflows from water treatment facilities, land disposal from septic tanks and landfills, agricultural and urban runoff, and atmospheric deposition.4 To illustrate the issues related to water contaminants, we review information about a familiar toxicant, methylmercury (MeHg).
Humans are exposed to the harmful effects of methylmercury mostly through fish and seafood consumption. Elemental mercury enters our lakes, streams, and oceans from natural and mostly manmade sources, such as air pollution and industrial waste and discharge. Microorganisms in the sediment convert the mercury to organic methylmercury, a compound that enters the aquatic food chain where it is bioaccumulated and biomagnified as it moves up the food ladder.
Predator species, such as tuna, shark, and swordfish, accumulate the greatest amounts of methylmercury; several freshwater species also accumulate methylmercury depending on the mercuric content of the local body of water. In general, larger fish with longer life spans harbor greater amounts of mercury. The US Geological Survey (USGS) recently released a report indicating that 27% of the freshwater fish sampled across the country had mercury levels that exceeded the EPA safe limit.5
Once methylmercury is consumed, it is highly lipid soluble, absorbed through the gastrointestinal tract, and readily crosses the blood-brain barrier. During pregnancy, the compound can cross the placental barrier, allowing fetal levels to equal or exceed maternal concentrations. Methylmercury also appears in human breast milk and can be passed on to nursing infants. The ill effects of mercury are greatest on the pre- and postnatal developing central nervous system (CNS).
The effects of high-level maternal exposures on fetal development are well documented. In the two most prominent cases of high level maternal MeHg poisoning in Minimata, Japan, and in Northern Iraq, even although mothers showed no ill effects and infants appeared normal at birth, by 3 years, most children had profound language, motor, and cognitive deficits.6
Evidence for low-level maternal exposure and high-level postnatal child exposure also present concerns regarding neurologic development. Two large epidemiologic studies6–9 have documented negative effects of mercury on cognitive development (reduced performance on neurobehavioral tests, including tests of attention, fine-motor function, language, visual-spatial abilities, and verbal memory).
A third study using a comparable design did not fully support these conclusions.10 Differences among these studies may be due to different exposure levels and/or effect modifiers that were not controlled for or analyzed.11
Coal combustion is the greatest source of mercury contamination worldwide.12 Although three times more mercury is present in the environment today than in pre-industrial times, levels in the US are now less than half of those present in 1950 as a result of reduction and regulation of mercury use (eg, EPA regulation of municipal and hazardous waste combustors); this is an example of how policy can lead to significant environmental improvement.
Unfortunately, mercury emissions are now on the rise worldwide due to construction of coal-fired power plants as nations become more industrialized, especially in Asia.13 A recent study documented levels of mercury in the North Pacific Ocean to be 30% higher than those measured in the mid-1990s, with evidence suggesting the increase was due to long-range transport of emissions from Asian sources.14 Therefore, it is probable that mercury pollution originating in any country where emission controls are largely unregulated will have health effects around the globe.
What Pediatricians Can Do
The 2000 report of the National Research Council (NRC) concluded that the risk of adverse effects for most of the US population is low, but individuals with high MeHg exposures from frequent fish consumption have little or no margin of safety (ie, exposures of high-end consumers are close to those with observable adverse effects).15 Therefore, it is important that patients have accurate information about fish consumption and the risks methylmercury may pose.
The public’s awareness and knowledge about fish contamination may vary. Seventy percent of respondents in one study knew of risks associated with fish, but their specific information was often inaccurate or deficient, and unfortunately respondents felt they did not need further information.16 Pediatricians can assess exposure (eg, by evaluating frequency and kind of fish intake), and either directly provide or point to sources of information about MeHg levels in commercially available seafood (wild caught and farm-raised) and locally caught fish, coupled with a food frequency assessment. The FDA publishes a list of mercury levels of commercial fish (see Sidebar).
Mercury Levels for Fish
FDA mercury levels for commercial fish are available at www.fda.gov/Food/Food-Safety/Product-SpecificInformation/Seafood/FoodbornePathogensContaminants/Methylmercury/ucm115644.htm
.For individuals and populations who consume sport-caught fish, assuring awareness of advisories is important. The EPA maintains a fish advisory Web page, which links to individual state’s listings: water.epa.gov/scitech/swguidance/fishshellfish/fishadvisories/advisories_index.cfm
A national list of local fish advisories regarding consumption recommendations is published by the EPA (see Sidebar). The local information takes on added importance given the results of the recent USGS study illustrating the magnitude of the mercury problem in our country’s lakes and steams.5 Consumer safety companies, such as Safe Harbor, are also active in some communities, testing and certifying that seafood products have mercury levels below the FDA limits ( www.safeharborfoods.com).
Limiting fish consumption presents a dilemma for health care professionals due to the many health benefits that eating fish can provide a population. The consumption of fish with lower MeHg concentrations should continue to be encouraged.15 Pediatricians individually and through professional and advocacy organizations have the opportunity to encourage policymakers to pass regulations limiting mercury discharge at the national and international level. The EPA attempted to cap mercury emissions for new and existing power plants in 2005 by establishing the Clean Air Mercury Rule (CAMR).17 However, aspects of this rule were opposed by organizations (including states) who saw the rule as running counter to the intent of the Clear Air Act. In early 2008, the US Court of Appeals voided CAMR. The EPA is now in the process of developing emissions standards for power plants under the Clear Air Act (Section 112), consistent with the court’s ruling ( www.epa.gov/camr).
Exposure to Lead
Childhood lead poisoning, a public health issue for over a century, is associated with protracted physical development;18 gastrointestinal disorders;19 decreased cognitive function;20,21 antisocial behavior;22 delinquency;23 and in severe cases, death.24 Due to lead’s varied uses and persistence in the environment, childhood lead poisoning remains a major environmental health problem in the United States.25
Lead poisoning is currently defined as a blood lead level (BLL) greater or equal to 10 mcg/dL, although deleterious effects at lower levels have been documented.26 A threshold value below which lead has no adverse developmental effects, has not been identified.27 Federal mandates removing lead from gasoline and interior paint have resulted in a decline of childhood BLLs over the past 50 years. The proportion of children 1 to 5 years with blood lead levels greater or equal to 10 mcg/dL declined from 88% during the phase-out of leaded gas in the late 1970s to 2.2% in 1999–2000.28 The decline in lead levels demonstrates the potential for policy and regulations to improve the living environment.
Lead-based paint remains the most common high-dose source of lead exposure for preschool children. Nationwide, about 3 million tons of lead remain in approximately 57 million occupied private housing units built before 1980, representing 74% of such housing. Of particular concern are the 3.8 million housing units occupied by young children believed to contain lead paint in unsound condition.
Abraded lead paint on friction surfaces, such as interior and exterior window components, is inhaled or ingested via hand-to-mouth activity and has been identified as a major contributor to the total lead body burden in children.29 Because lead does not dissipate, biodegrade, or decay, the lead deposited into dust and soil becomes a long-term source of exposure.
Young children, particularly those younger than 2 years, are most susceptible to the effects of lead due to the rapid ongoing development of the CNS, the high degree of lead absorption in the body,30 and hand-to-mouth and exploring behaviors characteristic of this age. Black children and Latino children are more vulnerable to the deleterious effects of lead,31,32 even after accounting for social, behavioral, nutritional, and environmental factors.33
One of the strongest environmental factors for high levels of lead poisoning is a large proportion of older housing stock in a community.34 Lower housing values, lower proportion of owner-occupied housing, and higher proportion of vacant housing are all risk factors for lead exposure.35 National data indicate that children who are black, impoverished, and live in housing built before 1950, are at highest risk for lead poisoning.33
The Role of the Pediatrician
Lead poisoning is completely preventable. Pediatricians and other physicians have been directly involved in federal and state level efforts to ban lead in the environment. Pediatricians were also heavily represented on the Centers for Disease Control and Prevention (CDC) work group that released the 2005 revision of the document Preventing Lead Poisoning in Young Children.36 In the office setting, appropriate screening and anticipatory guidance will continue to be valuable elements aimed at reducing a child’s lead exposure.
Secondary screening of high-risk groups has attempted to limit further CNS damage in children already exposed to lead and prevent other children from exposure to the same lead sources.37 Because most children exposed to lead are clinically asymptomatic, 38 BLL testing is necessary to identify children with elevated blood lead levels (EBLL) (greater or equal to 20 mcg/dL or two BLLs greater or equal to 15 mcg/dL drawn less than 90 days apart) to implement environmental remediation, education, and case management. Continuous monitoring of children with EBLL is used to assure that no new exposures occur.
Because not all children are at equal risk for lead exposure, the American Academy of Pediatrics (AAP) recommends use of strategies that target children in high-risk communities39 where greater than 27% of the homes were built before 1950; and the percentage of children with EBLL is greater than 12%.40 Federal policy requires that all children enrolled in Medicaid receive BLL-screening tests at 12 and 24 months and that BLL screening be performed for children 36 to 72 months who have not been screened previously.41
Despite this mandate, BLL-screening rates for Medicaid-enrolled children have been less than 20%,42,43 and testing rates for high-risk children remain low.44 Consequently, the CDC has requested that local and state health officials use local-community-wide data (eg, BLL prevalence, housing age, and poverty status) to develop plans for BLL screening for their jurisdictions.38
Screening of high risk, older housing units would be the most effective primary prevention measure, avoiding initial lead exposure during early childhood. Although appropriate housing unit lead control is expensive, the cost is more than offset by medical and future productivity benefits of avoiding childhood lead ingestions.45 Pediatricians can continue to advocate for local, state, and federal support of lead abatement programs especially in known high-risk settings.
Environmental tobacco smoke (ETS) is among the most important environmental problems facing children in our society and around the world. The health effects of ETS were first described in the 1972 US Surgeon General’s (SG) Report and expanded in subsequent SG reports.46–48 In 1992, the EPA classified ETS as a class-A carcinogen, and in 1999 WHO declared ETS “… a real and substantial threat to child health … [with] almost half of the world’s children … regularly exposed to ETS [with] most hav[ing] no choice in the matter … ”49
The 2006 SG report concluded that ETS causes premature death and disease in children who do not smoke and slows lung growth.46 Prenatal smoking exposure is associated with lower birth weight, preterm birth, sudden infant death syndrome (SIDS), and (over the long-term) childhood cancers.46 Postnatally, parental (particularly maternal) smoking causes increased lower respiratory illnesses (eg, bronchitis and pneumonia) especially in children younger than 2 years, and middle ear disease, asthma, and respiratory symptoms in schoolchildren.46
Mainstream smoke (exhaled by the smoker) and sidestream smoke (released by the smoldering cigarette) contain particles and gases generated by the combustion of tobacco, paper, and additives and toxic or carcinogenic chemicals within the cigarette. There is no “safe” level of exposure to ETS. Moreover, the ETS risks can only be controlled by eliminating smoking in indoor spaces. Separating smokers and nonsmokers, cleaning air, or ventilating buildings are ineffective.46
Most children have detectable levels of serum cotinine (a metabolite of nicotine used as a marker for smoke exposure).50 Cotinine levels in 4- to 18-year-old children decreased between 1988 to 1991 through 2002, but declines were around 15% less than those observed in adults.50,51 Nearly 60% of children are still exposed to ETS in their homes, 33% in vehicles, 23% in restaurants, and 10% in offices or factories.52
More blacks (94%) than whites (84%) or Mexican-Americans (78%) have detectable cotinine levels, and disparities between blacks and other groups have increased.51 A significant percentage of young children of low socioeconomic living in the Midwest surveyed by the National Health and Nutrition Examination Survey (NHANES) had detectable serum cotinine levels.52–54
How Pediatricians Can Help
More pediatricians than family medicine physicians ask about rules prohibiting smoking in the home (38% compared with 29%) during an office visit. However, fewer than half of physicians from either specialty counseled smoking parents about the dangers of ETS or provided advice to parents about quitting.55 Pediatricians affect the ETS levels of children by integrating inquiries about parental and household smoking history, providing counseling that includes discussion of the dangers of ETS to child health, and counseling or referring parents to smoking cessation programs.56 Health insurance payers are strongly encouraged to provide financial incentives for these prevention encounters to help remove the resource barriers physicians face in providing these services to families.
Major medical associations (including the American Medical Association, AAP, American Academy of Family Physicians, and the College of Obstetrics and Gynecology) have active, influential federal and state level government affairs departments providing an avenue for pediatricians to influence policy. Policies limiting ETS have been very effective.
For example, cigarette prices and taxes, and stronger restrictions on smoking in workplaces, restaurants, and child care centers, have been shown to be associated with reductions in SIDS cases.57 The American Lung Association maintains a database (State Legislated Actions on Tobacco Issues, SLATI) including tobacco control laws and policies instituted in 48 states ( slati.lungusa.org/states.asp). Policies with the greatest potential effects on ETS are those affecting clean indoor air.58 The AAP has a long-standing policy urging pediatricians and state AAP chapters to lobby for the passage of smoke-free laws in their states.56
Asthma is the most common chronic disease of childhood.59 In the United States, asthma is the primary reason for missed school days60 and noninjury hospitalization61 and is the single most prevalent cause of childhood disability.62 Estimates from national prevalence surveys suggest that approximately 7% of children younger than 18 years have asthma.63 Data from the NHANES have indicated that childhood asthma prevalence increased from 3.5% in 1980 to 7.5% in 1995 and has remained stable since 2000.64
Asthma is a heterogeneous condition. One of the main obstacles in understanding its natural history has been the lack of well-defined markers for the different disease phenotypes grouped under this common label.65 More than one-half the cases of persistent asthma start before 6 years;66 young children are more susceptible than adults to induction of asthma by environmental factors.67 Early clinical observations on asthma documented its strong association with the presence of IgE antibodies directed against common environmental allergens.68
Although the precise environmental determinants of asthma are not clear, there is strong evidence that asthma, like atopy, has a genetic component. It is likely that gene-environment interactions within a specific temporal window, most likely during early childhood or infancy, contribute significantly to the development of asthma.
Because of the myriad exposures implicated in asthma etiology, such as airborne allergens,69 viral infections,69 environmental tobacco smoke,70 and ambient air pollution, 71 and the multitude of genes involved in immunological and developmental pathways, it is difficult to define precise exposures and genes involved in this process. The array of asthma phenotypes, as well as the complex nature of the disease, suggests that numerous biological and environmental factors are implicated in this process.
Although several studies indicate that the prevalence of childhood asthma is consistent among different racial and ethnic groups,63 asthma-related morbidity, most often defined as missed days of school, outpatient emergency department (ED) utilization, and hospitalization, is disproportionately high among black children who reside in urban areas, especially those of low socioeconomic status.72
Air pollution in urban areas has created a significant amount of concern in the environmental justice movement due to the large number of minority and low-income residents who live in areas with poor air quality.73 Five of the six key air pollutants [ozone (O3), particulate matter (PM), sulfur dioxide (SO2), nitrogen dioxide (NO2), and carbon monoxide (CO)] interfere with oxygen delivery and are therefore of particular concern for asthmatic populations.74
The lack of a clear physiological and immunological characterization of asthma etiology and the asthma phenotype in young children has implications for the clinical diagnosis and management of pediatric asthma. However, as with most chronic diseases, this has not precluded the conduct of epidemiologic and clinical research on disease management and mitigation of the physiological and psychological effects of the disease.
Identification and treatment of impaired quality of life is recognized as an important component of asthma management. International guidelines stipulate that asthma treatment should improve the asthmatic’s clinical status and improve an individual’s ability to “feel and function better in their day-to-day life.”75
Asthma-related morbidity and mortality are, in principle, preventable when patients and families are educated about the disease and have access to high quality health care. It is estimated that 90% of the day-to-day control of asthma is in the hands of the patient and his/her parents; therefore, self-management must be the primary focus of efforts to control asthma-related morbidity.76
Guidelines established by the National Asthma Education and Prevention Program (NAEPP) and the Global Initiative for Asthma (GINA) indicate that pharmacotherapy, knowledge, and recognition of asthma triggers, and a working partnership with a primary care provider (PCP), can decrease asthma-related morbidity and have been demonstrated to improve quality of life for children with asthma.75
Despite evidence that asthma control is an achievable outcome, poor disease management for children persists, particularly for those residing in urban communities.77 PCP are often the main source for initial asthma diagnosis, education, and symptom monitoring. Current data support the crucial role of the PCP, particularly for urban children.78 Reliance on outpatient emergency care as a primary source of health care in urban populations interferes with the development of partnerships between clinicians and caretakers and limits opportunities for asthma education.79
The expanding body of clinical recommendations along with the complexity of the NAEPP guidelines may impede effective implementation into practice.80 In addition, well-trained physicians who are able to implement guidelines may encounter structural barriers to implementation, such as lack of time, lack of budgetary control for resources (ie, spirometers), and restrictions on referrals to specialists.81
As the prevalence of childhood asthma increases, physician involvement in asthma prevention and management activities has also increased. Many avenues exist for physicians, especially pediatricians, to become involved in efforts to shape policies that may alleviate the burden of asthma.
The Children’s Health Alliance of Wisconsin organized the Wisconsin Asthma Coalition, whose executive committee is chaired by a pediatrician/allergist. This coalition’s 2009–2014 plan includes public policy recommendations including support of legislation to ban smoking in public and indoor work places and to limit idling of school buses and other diesel-powered vehicles.82
In 1997, the Wisconsin Medical Society lobbied in support of 1997 Assembly Bill 783, allowing an asthmatic student, while in school, to possess and use a metered dose inhaler or dry powder inhaler if the student uses the inhaler before exercise to prevent the onset of asthmatic symptoms or uses the inhaler to alleviate asthmatic symptoms. These efforts contributed to the passage of this bill and its enactment into law as 1997 Wisconsin Act 77.83
Environmental health exposures contribute to a significant disease burden in pediatric populations. These brief examples of potentially detrimental water, land, and air substance exposures demonstrate the need for increased attention to environmentally-mediated diseases in the clinical setting.
The AAP Committee on Environmental Health (COEH) has published policy statements for common environmental exposures, including MeHg, lead, ETS, and indoor and outdoor air pollution.84 These recommendations emphasize the role of the physician as educator conveying actionable recommendations to patients and their families that will mitigate the negative health effects of these contacts. When followed, these steps may motivate patients to limit exposures, lead to a reduction in environmental-health related morbidity and mortality, and raise the quality of life of families and children.
Pediatricians should make focused environmental health questions a routine part of the clinical history85 and should attempt to ensure that environmental health messages — such as avoidance of environmental tobacco smoke — are underscored during office visits.
Although the examples presented in this overview describe exposures and outcomes from varied etiologies, the burden of disease disproportionately effects low-income populations. Including inquiries relating to environmental exposures in patient visits may help reduce these health disparities.
Even when small reductions in exposures do not discernibly improve health on an individual level, aggregated over a population, reduction in environmental exposures and diseases will have a meaningful effect on public health.86
Pediatricians have been instrumental in the development and implementation of policies that have successfully reduced harmful environmental contacts. Clinicians should not underestimate the potential effect and momentum that local ordinances targeting environmental health exposures can have as demonstration projects.
For example, passage of clean-indoor air legislation in many areas was initiated by local grassroots movements. At the local and state level, pediatricians can continue to use their scientific knowledge and clinical experience to encourage the development and support of environmental health policy, in particular by providing relevant clinical anecdotes as part of compelling testimony. The respect attached to the medical profession lends substantial weight to these advocacy efforts aimed at bettering the health of children in the community.
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