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American Journal of Public Health logoLink to American Journal of Public Health
. 2011 Dec;101(Suppl 1):S53–S63. doi: 10.2105/AJPH.2011.300121

Disproportionate Exposures in Environmental Justice and Other Populations: The Importance of Outliers

Michael Gochfeld 1, Joanna Burger 1,
PMCID: PMC3222496  PMID: 21551384

Abstract

We examined traditional environmental justice populations and other groups whose exposure to contaminants is often disproportionately high. Risk assessment methods may not identify these populations, particularly if they are spatially dispersed.

We suggest using a National Health and Nutrition Examination Survey approach to oversample minority communities and develop methods for assessing exposure at different distances from pollution sources; publishing arithmetic and geometric means and full distributions for minority populations; and paying particular attention to high-end exposures.

Means may sufficiently characterize populations as a whole but are inadequate in identifying vulnerable groups and subgroups. The number of individuals above the 95th percentile of any distribution may be small and unrepresentative, but these outliers are the ones who need to be protected.


Environmental risks are not uniformly distributed across groups of people. Age, poverty, and minority status place some groups at a disproportionately high risk for environmental disease. Such groups are exposed to hazardous chemicals or conditions at levels well above those for the general populations.1,2 These exposures may be high-end exposures (> 95th or 99th percentile) to common agents or exposures the general population does not encounter. In traditional risk assessment and management, outliers are excluded or log-transformed; however, special attention should be paid to them.

We discuss populations with high-end, unique exposure pathways (children, Native Americans, minorities, rural and urban poor), whose risk from combined exposures (chemical, physical, psychosocial) is likely to be underestimated by risk assessment practices, and examine their contribution to health disparities. Some of these populations are traditionally recognized environmental justice communities. We build on our conceptual model for unique exposure pathways, and we also make specific recommendations regarding how a National Health and Nutrition Examination Survey approach can focus attention on addressing information disparities.

We used Medline searches to identify the articles included in this review, using keywords for vulnerable populations, tables of contents searches for environmental justice in biomedical journals, US Environmental Protection Agency documents,1 and our cumulative research experience. More search details are provided in our other article in this issue Our review is also based on our work with environmental health, exposure, and risk assessment.

BACKGROUND CONCEPTS

Risk assessment is evolving to improve toxicological basis, exposure assessment, and quantitative approaches,35 with increasing attention paid to mixtures and cumulative exposures.6 Here, we distinguish vulnerability (differential probability of exposure) from susceptibility (differential probability of experiencing adverse effects from exposure). Factors that contribute to differential exposure and response interact in complex ways involving state of health and nutrition, hazardous occupations, and hazardous behaviors such as smoking or lack of exercise.7 For example, children with asthma from poor minority communities may be particularly sensitive to volatile organics.8,9 We highlight other factors that interact to increase minority and low-income populations’ potential for higher exposure (vulnerability) or high responsiveness (susceptibility) to environmental toxics that are under the purview of the Environmental Protection Agency (EPA).

Disparities in access to health information and health care are important aspects of the disproportionate burden faced by environmental justice communities. Poor access to health information and health care means less health promotion, less risk avoidance, a less healthy diet, and more adverse conditions that increase susceptibility to exposure. Delayed recognition of exposure, diagnosis, and treatment allows effects to accumulate.10 For example, Pacific Northwest Tribes have experienced greater delays in access to medical care, in addition to lower quality care.11 Data have suggested that their cancer incidence is higher than the national average, and their higher mortality may be the result of late-stage diagnosis and limited access to state-of-the-art care.11 Limited access to medical care is well recognized12 for Native Americans generally, for poor rural communities,13 and for minority communities,14 which adds to their already disproportionate risk of exposure to chemicals. In New York City, disparities in health outcomes from exposure to air pollution relate directly to less access to care as a result of socioeconomic status.15

Poor and minority groups experience unusually high exposures in home and neighborhood. They are also disproportionately affected by hazardous occupational exposures. Recent immigrants have low-paying, nonunion, and hazardous jobs, occupy crowded and deteriorating housing, experience economic and social stressors, and have less access to information and health care.16 They are disproportionately exposed at work and are more likely to bring chemicals home on their clothing17 than workers in factories with strong unions, who change out of work clothes and shower before leaving work.18

Smoking intersects with other risk factors, such as poverty and low educational level. Smoking is about 2 to 4 times more prevalent among those with less than a high school education than among college-educated people. Tobacco companies have targeted children and minorities to increase the number of new smokers.19,20 Black men (27.1%) smoke more than non-Hispanic White men (24.0%) or Hispanic men (19.9%); for Black women, the rate was 18% higher; for non-Hispanic White women, 19.6%; and for Hispanic women, 10%.19, 21 Puerto Ricans had much higher smoking rates than Cubans or Dominicans. The highest smoking rate was among American Indians (32%).21

UNIQUELY EXPOSED POPULATIONS AND ROUTES OF EXPOSURE

People with unique exposure pathways include children,22,23 farm and migrant workers,2426 urban poor populations,2729 rural or isolated populations,30,31 Native Americans and Alaskan Natives, and minorities. These groups are often, but not always, immersed in a dominant culture. For example, Aleuts live in small communities separated from mainland Alaska by hundreds of miles,32,33 and some poor, rural communities in Appalachia face disproportionately more environmental hazards.34 Even in urban areas, low-income and minority communities may be found in otherwise affluent areas.35

The issues are as diverse as low group population,32 inordinately high fish consumption rates (e.g., Native Americans),36,37 high consumption rates of other subsistence foods,33 high exposure to pesticides,38,39 or cultural practices.4042 Environmental risk factors include hazardous waste, indoor toxins, indoor or outdoor air pollution, water quality, noise, crowding, housing quality, school quality, work exposure, and blighted neighborhoods.43 We describe major groups of environmental justice populations facing unique exposures, beginning with children.

Children

Children should not be considered small adults in terms of exposure, dose, or response.44,45 They may absorb more contaminants (e.g. lead) and metabolize differently; also, their developing nervous systems are more susceptible to chemicals. From conception through adolescence, children have critical developmental windows when the nervous system is more susceptible to damage. Children from low-income and minority families are more likely to be at risk of exposure because they (1) spend more time playing on contaminated soil than children from higher-income families, (2) spend more time in houses that have lead paint or high dust levels, (3) may be exposed to higher levels of contaminants in utero and in breast milk because their mothers are also disproportionately exposed, and (4) have inadequate diets that may increase the absorption of toxic chemicals from their digestive system.

Children in rural areas may live close to industrial sites,46 mines,47 smelters,48 and waste sites and may be unduly exposed during exploration of their surroundings.49,50 Infants and toddlers are differentially exposed when they spend time on the floor or ground putting their hands or objects in their mouths.51,52 Crawling also provides an opportunity to ingest dust. In a Texas farming community, the rate of contact with dirt or grass and the rate of hand-to-mouth activities varied by age; children had higher rates of exposure indoors than outdoors52 (Table 1). Freeman et al.53 found similar rates of hand-to-mouth activities in children exposed to lead. Soil ingestion by young children is usually the driver in risk assessment scenarios. Kimbrough et al.54 used values of 100 milligrams to 10 grams per day for daily deposition of soil containing 2,3,7,8-tetrachloro-dibenzodioxin on skin surfaces, and others have provided distributions for soil ingestion (mean = 14 mg/day).49,55

TABLE 1.

Contact Behavior of Infants and Children in a Texas Farming Community: 2000

Behavior Infants, % or Mean (SD) Aged 1 Year, % or Mean (SD) Aged 2 Years, % or Mean (SD) Preschool, % or Mean (SD)
Assessed via questionnaire (% of time having contact)a
    Dirt 15.7 54.5 66.7 100
    Grass 8.3 36.4 44.4 100
Assessed via videotaping (hourly frequency)a
    Hand to mouth 19.8 (14.5) 15.8 (8.7) 11.9 (9.3) 22.1 (22.1)
    Object to mouth 24.4 (11.6) 9.8 (6.3) 7.8 (5.8) 10.1 (12.4)
    Food to mouth 10.8 (9.0) 17.2 (14.0) 14.7 (10.9) 15.7 (11.8)
Assessed via videotaping (% of time on floor)a 11 (10) 8 (5) 9 (4)
a

Data from Black et al. 2005.52

An example of how children may be differentially exposed to environmental toxins is children's exposure to lead. Lead poisoning in children is a classic example of failure and success in public health.56 In the United States, the days of emergency admissions for lead encephalopathy with blood lead levels exceeding 100 micrograms per deciliter have largely passed, and the level that defines lead poisoning in children has been lowered to 10 micrograms per deciliter. Declines in blood lead levels in the United States tracked declines in leaded gasoline;57 the number of children aged 1 to 5 years with blood lead levels exceeding 10 micrograms per deciliter has declined nationwide from more than 50% in the 1970s to 1.6% in 2002 but has remained higher than 5% in some cities.58 Researchers have disagreed over whether a blood level of 10 micrograms of lead per deciliter is adequately protective.59,60 Early childhood blood lead levels and reading achievement showed an evident negative association at 5 micrograms per deciliter,61 and children with a lifetime average blood lead level of 5 to 9.9 micrograms per deciliter showed a 4.9-point-lower performance on full-scale IQ.62

Black children have higher blood lead levels than White children.6365 Poor and minority families are more likely to live in older, deteriorated housing in which lead chips and dust as well as lead water pipes are the main culprits. National Health and Nutrition Examination Survey II data (1991–1994) for 2392 children aged 1 to 5 years showed higher blood lead levels for low-income children (8%; lead > 10 ug/dL), non-Hispanic Black children (11.2%), and children who lived in housing built before 1946 (8.6%) compared with about 2% for children in other categories.65 In a Rochester, New York, study,66 2-year old Black children had a mean blood lead level of 9.6 micrograms per deciliter compared with 4.8 micrograms per deciliter for White children, but 47% exceeded 10 micrograms per deciliter compared with 6% of White children. Immigrant children may also be disproportionately exposed to lead. In New York City, children with blood lead levels higher than 10 micrograms per deciliter were 11 times more likely to have lived in the United States for less than 6 months.67 Other risk factors were residence in pre-1950 buildings, living in buildings with only 1 or 2 units, putting fingers in the mouth, and eating nonfood items. Parent report of peeling paint was not a significant predictor.67 In Chicago, lead levels higher than 10 micrograms per deciliter occurred in 30% of children and were inversely related to caretaker's educational level in Black children.63 Moreover, Edwards et al.68 found blood lead levels higher than 10 micrograms per deciliter in children aged 1.3 years and older living in neighborhoods in which lead levels in water were elevated, which was also true in the Rochester study.66 Racial disparities in childhood lead exposure persist, and screening criteria need to target families with multiple risk factors for lead exposure and toxicity (older housing, nutrition, iron-deficiency anemia).

Native Americans

Native Americans are a unique exposure group because the more than 500 different tribes have different mores, economical and social structures, and environmental conditions. First Nation environmentalists have viewed health issues broadly and included cultural issues. Exposure scenarios developed for the Yakama69 and the Confederated Tribes of the Umatilla Indian Reservation37,70,71 of Washington State illustrate unusual exposures. Harper et al.72 developed a landmark guidance manual for tribal exposure scenarios and risk assessments for Native Americans. It is a transferable resource for assessments conducted for other minority and ethnic groups. In developing exposure pathway scenarios for Native Americans, important aspects are recognizing their unique activities, the frequency and duration of these activities, and the holistic nature of their ecocultural dependency webs (see the box on the previous page). American Indian activities include fishing; hunting; gathering materials used for mats, baskets, and bags and for other uses; consumption and use of water; time spent outdoors; cultural activities; memorials; and ceremonies.69 Sweat baths are a unique exposure pathway because of their intensity and duration.72 Although several exposure pathways have been identified for Native Americans, few studies have examined human tissue levels in relationship to those pathways.

Factors to Consider in Examining Pathways for High-End Exposure for Groups With a Subsistence Lifestyle, Recreationalists, and Native Americans With a Traditional Lifestyle

Components of the Activity Special Exposure Considerations of the Activity
Hunting
Preparation for hunting Are products for food, drink, implements, cosmetics, ceremonies, or medicines?
Hiking to hunting site What are the terrain types or aquatic conditions?
Canoeing or boating to site Is game butchered on site or brought back to land or to home?
Conducting scouting trips What are the exertion levels for and time spent in each activity?
Setting traplines What are the total number of exposure pathways of each activity (inhalation, dermal, ingestion)
Building blinds Do people live on a boat at sea or in other places?
Capturing or killing prey How much is frozen, smoked, or freeze dried for later consumption?
Field dressing food
Packing food
Hauling food
Cutting or storing food
Drying or smoking food
Preparing hides, skins, or antlers for decorations
Returning remains to nature
Fishing
Preparations for fishing What are the products involved?
Canoeing or boating to site What types of terrain are crossed to get there, and what are the aquatic conditions for fishing?
Hiking to collecting site Are fish butchered on site or brought back to home, camp, or a village?
Building weirs or traps Contents of fish guts can influence exposure
Making or repairing nets What are the exertion level and time spent in each activity?
Making or repairing poles What are the total number of exposure pathways of each activity?
Constructing drying racks Are fish given to neighbors or friends?
Fishing itself
Cleaning or storing fish
Drying fish
Returning remains to nature
Gathering
Preparing materials What are the products?
Canoeing or boating to site Do they involve gardening, and if so what level?
Hiking to collecting site What are the terrain types?
Searching for materials What are the exertion levels and time spent in each activity?
Collecting materials Is soil left on the products?
Carrying materials back to home What are the total number of exposure pathways for each activity?
Preparing materials to store
Preparing materials to dry or package
Returning remains to nature
Food, herb, or medicine preparation
Basket making What are the materials or structures constructed?
Building drying racks or smoking sites Where are these built?
Separating parts of plants, fish, or game What are the exertion levels and time spent in each activity?
Making storage buildings or smoke houses What are the total number of exposure pathways for each activity?
Spreading materials around medicines or herbs (such as mercury) Are there unique ceremonial activities (such as use of mercury)?
Creating amulets (e.g., of mercury)
Camping or hiking
Recreational What are the time constraints?
For hunting or fishing How many days and nights are involved?
Set up time What are the ages of the participants?
Time in the field Where does it take place?
Use of natural materials (food or fiber) How many different habitats are used?
Involvement in multiple activities What are the exposures for each activity on these trips?
What is consumed on the trips versus brought home for immediate or future use?
What is given away to others?

Note. Determining exposure pathways often involves dissecting major activity categories (for all ages and genders). For all of these activities, exposure pathway considerations involved each individual's age and stage (gender, life stage such as pregnancy), number of times per day (or other time period), duration of activities, duration of seasonal and lifetime exposure, and overnight or daily activities. Each pattern within an activity type is a potential exposure pathway (involving inhalation, ingestion, or dermal exposure).

Sources. Ridolfi69; Harper et al.72; Burger et al.73; Burger and Gochfeld144; and unpublished data.

Other major exposure pathways for Native Americans and Alaskan Natives include consumption of plants, fish, and wildlife (see the box on the previous page). Native Americans’ hunting and fishing rates can be very high compared with those of other groups (although such high rates are not limited to Native Americans).74 Exposure occurs not only because of Native Americans’ increased consumption rates but because of the higher diversity in the foods they eat (many kinds of fish, game, roots, berries, shoots, and leaves). Patterns differ among tribes, depending on where they live, food use, cooking and preparation traditions, parts consumed, and ratio of river-bottom to upland resources.75 Native peoples see subsistence living as part of their culture, not as a reflection of necessity, poverty, or the minimum amount of food necessary to support life.72

Richardson and Currie76 found gender-related differences in fish consumption in American Indians from Ontario (geometric means = 19 g/day for men and 14 g/day for women), with the highest rates of consumption in summer and the lowest rates in winter. Fish consumption increased with latitude, isolation, and age (older people ate more fish). For pregnant women, several months of high consumption can lead to significantly different risk. DeWeese et al. 77 found a mean monthly fish consumption of 121 grams per day for April, 113.5 grams per day for May, and 30 grams per day for January through March. Although the geometric mean for women was 14 grams per day, the arithmetic mean was 27.7 grams per day.76 Moreover, the reported geometric mean hair mercury levels of 2.7 micrograms per gram (men) and 2.1 micrograms per gram (women) obscured the fact that mercury levels in some individuals of both genders exceeded 30 micrograms per gram,76 a level consistent with severe methylmercury poisoning.

Higher consumption of fish, seal, and seal liver (which are linked to increased levels of mercury in hair) was associated with lower socioeconomic status in the Inuit, whereas consumption of whale was uniform across economic classes.78 Women increased their consumption of fish and seal during pregnancy and averaged as many as 14.2 fish meals per month, 0.6 whale meals per month, and 0.8 seal meals per month. Traditional foods of the Dene and Metis in the Northwest Territories (Canada) were consumed on 65% of days (48 food types).79 Studies of Native Americans’ consumption rates can be used to understand both the breadth and the variation of exposure (Table 2). Traditional consumption rates for Native Americans were once much higher than they are now; current consumption rates are suppressed partly because of contamination in waterways,75 which suggests that consumption may increase if this contamination declines. Thus, those assessing exposure need to consider the potential for future increased consumption rates when developing exposure risk scenarios, setting water quality standards, and developing fish consumption advisories.

TABLE 2.

Fish Consumption Reported for Native American Versus EPA Exposure Assumptions: 2005

Source Average Daily Intake, g/d (kg/y) Daily MeHg Intake, Fish With 0.3 ppm (μg/d) Daily MeHg/kg Body Weight (Assumed to Be 70 kg)
EPA averagea rate, US population 6.5 (2.4) 1.9 0.03
EPA default consumption rate80 17.5 (6.4) 5.2 0.08
EPA alternative recommended rate, two 6-oz meals/wk 48.5 (17.7) 0.21
EPA consumption rate80
    Subsistence fishers 142.4 (52.0) 42.7 0.61
    Pregnant women 165.5 (60.4) 49.7 0.71
American Indians, Ontario76
    Men 19 (6.9) 5.7 0.08
    Women 14 (5.1) 4.2 0.06
Native Americans, MI81 24.3 (8.9) 7.3 0.10
Tulalip and Squaxin Tribes, Puget Sound, WA82 60.72b (22.2) 18.2 0.26
Columbia River, WA, tribes36 63.2 (23.1) 19.0 0.27
Anishinaabe, Great Lakes77
    December 15.1 (5.5) 4.5 0.06
    Aprilc 121.1 (44.2) 36.3 0.52
Columbia River, median for 1950s83 350 (128) 105 1.5
Columbia River, 99th percentile36 389 (142) 117 1.7
CTUIR traditional rate37 454 (156) 136 1.9
Historicd Yakama72,75 620 (226) 186 2.7

Note. CTUIR = Confederated Tribes of the Umatilla Indian Reservation; EPA = Environmental Protection Agency; MeHg = methylmercury.

a

EPA has established various assumption values for different fish types of fish consumers.

b

Both fish and shellfish.

c

Calculated from high rate for April for the tribe (× 227 g/meal).

d

Refers to what tribal members ate historically before contamination and other factors both suppressed the fish population and rendered them high in contaminants, resulting in lowered fish consumption.

Subsistence and Game or Sports Fishermen

Consumption of noncommercial food is a major route of exposure that can lead to adverse health outcomes for many Americans, as well as for environmental justice communities. These pathways need to be considered for other minority, low-income, and rural communities, as well as for children and Native Americans.

One of the main pathways for excessive exposure of minorities and low-income families is through consumption of wild-caught plants, fish, and game. For example, fishermen in Newark Bay, New Jersey, showed different patterns of exposure as a function of ethnicity and catch type.84 Whites had higher consumption of crabs (highly contaminated with polychlorinated biphenyls), but lower consumption of fish (highly contaminated with mercury); Asian Americans had the highest consumption of fish, but the lowest consumption of crabs. Blacks who ate both fish and crabs had higher consumption rates than other groups. Consumption rates for all groups decreased with income.84 Similarly, in South Carolina Blacks had higher consumption of wild-caught fish (high levels of mercury), whereas Whites had higher consumption of deer.85 Data on consumption rates for minority, low-income, and recreational fish consumers support the need for site-specific data on high-end consumers and outliers, including at least the 95th percentile of distributions (Table 3). These data show that uniformity is needed in the approach to gathering information on consumption of both wild-caught and commercial foods.

TABLE 3.

Fish Intake Reported for Other High-End Consumption Groups: 2000

Source/Subgroup Daily Intake g/d (kg/y) Daily MeHg Intake, Fish With 0.3 ppm (ug/d) Daily MeHg/kg Body Weight (Assumed to Be 70 kg)
EPA default consumption rate80 17.5 (6.4) 5.2 0.08
General population
General population, freshwater fish, Maine86 3.7 (1.3) 1.1 0.02
Sport fishers, Lake Ontario87 4.9; 17.9 from all sources (1.8) 1.5 0.02
US population, 48 states (all fish)88 15.6 (5.7) 4.7 0.07
General population, Lake Ontario87 17.9 (6.5) 5.4 0.08
General population, Louisana89 23.5 (8.6) 7.1 0.10
Recreational anglers, Indiana90
    All, range 16.4–32.3 (6.0–11.8) 4.9–9.7 0.07–0.14
    Minority 38.3 (14) 11.5 0.16
Angler population, Michigan,91 range 40.9–61.3 (14.9–22.4) 12.3–18.4 0.18–0.26
General population, New Jersey,92 mean ±SD 50.2 ±47 (18.3) 15.1 0.22
Recreational anglers, Washington93 52.8 (19.3) 15.9 0.23
    Marine fish 53 (19.3) 15.9 0.23
    Shellfish 25 (9.1) 7.5 0.11
    Freshwater94 10 (3.7) 3.0 0.04
Minority
Delaware95
    Black 15 (5.5) 4.5 0.06
    Asian 6 (2.2) 1.8 0.03
    Hispanic 3 (1.1) 0.9 0.01
Michigan81
    Native American 24.3 (8.9) 7.3 0.10
    Black 20.3 (7.4) 6.1 0.09
    White 17.9 (6.5) 5.4 0.08
San Francisco Bay, CA95
    Black 27 (9.9) 8.1 0.12
    Chinese 28 (10.2) 8.4 0.12
    Filipino 33 (12.0) 9.9 0.14
    Pacific Islander 38 (13.9) 11.4 0.16
    Asian 22 (8.0) 6.6 0.09
    Hispanic 22 (8.0) 6.6 0.09
New Jersey84
    Asian 52 (19.0) 15.6 0.22
    Hispanic 41 (15.0) 12.3 0.18
    White 27 (9.9) 8.1 0.12
    Black 23 (8.4) 6.9 0.10
South Carolina96
    Black men 70 (25.6) 21.0 0.30
    Black women 48 (17.5) 14.4 0.21
    White men 38 (13.9) 11.4 0.16
    White women 26 (9.5) 7.8 0.11
San Diego Bay, CA95
    Asian 82 (29.9) 24.6 0.35
    Filipino 50 (18.3) 15.0 0.21
    Hispanic 24 (8.8) 7.2 0.10
    White 11 (4.0) 3.3 0.05
Asians and Pacific Islanders, WA 117.2 (42.8) 35.2 0.50

Note. EPA = Environmental Protection Agency; MeHg = methylmercury. Some general population estimates from surveys with similar designs are included for comparison, but this list is not meant to be exhaustive.

Rural Populations

Disparities occur in rural areas,98 characterized as having low traffic, high dust levels, low lead levels, high pesticide levels, and uncertain water quality.99 Rural areas may be close to agriculture (farms, feedlots, swine facilities), where pesticide and animal waste exposures occur, and to mines, smelters, industries, and waste sites. Home-grown livestock and produce are a vector for pesticides, water pollutants, and soil contamination.100 Unusual exposure pathways for rural residents include consumption of self-caught fish and game, exposure to pesticides, and exposure to higher levels of mining materials, such as arsenic,100 and asbestos.101

People of low socioeconomic status may settle in rural areas in which housing is cheaper.102 Some rural populations are predominantly Black or Latino; although Latinos have mainly immigrated to cities, they have also moved to rural areas in which housing costs are low. Rural populations with a high proportion of African Americans have high mortality rates from injuries, suicide, and chronic obstructive lung disease.103

In isolated communities that have low population levels, people may be less willing to provide exposure information or unwilling to share cultural information.104,105 However, information gleaned from Aleut communities resulted in an understanding of the percentage of people who ate particular subsistence foods, although individual consumption rates were not obtained. Additionally, the low population level of many minority communities makes it difficult for residents (or researchers) to fathom a risk level of 1 in a million.

Farmers, Farm Workers, and Neighbors

Agriculture ranks among the most hazardous industries because of fatal and nonfatal injuries, work-related lung diseases, noise-induced hearing loss, skin diseases, and cancers associated with chemicals and prolonged sun exposure. Farming is one of the few industries in which the families are also at risk for injury, illness, and death and have measurable exposure to take-home pesticides.106 Farmers may have pesticide exposures similar to those of their hired help. Children living on farms may engage in farm work or have incidental exposure to chemicals around the farm. Neighbors may also experience exposure to pesticides from wind drift or runoff.

Most studies of farm workers have focused on occupational exposures,107 have not used biomarkers to assess exposure,108 or have not studied household exposure. Pesticides may be airborne or tracked into houses on clothes and shoes. Pesticides may be measured in air, water, soil, dust, and urine. Associations between organophosphate residues in house dust and organophosphate metabolites in the urine of farm workers and children were significantly positive. Urinary pesticide levels and symptoms are not always related, although headaches and blurred vision have been consistently reported.109

Proximity to farms may result in exposures and adverse outcomes. The amount of cropland within 750 meters of a house predicted the amount of herbicide residue on carpets.110 In California, pregnant mothers who lived within 500 meters of fields on which agricultural pesticides were applied (particularly dicofol and endosulfan) had a 6.1 odds ratio for having a child with autism spectrum disorder.111 In Washington, 13% of farm workers said they had been directly sprayed or dusted,112 as did Mexican farm workers in California.113 Poor minority schools in North Carolina were closer to swine confinement factories and were more likely to experience animal waste odors than were White high schools.114

Migrant Workers

Migrant workers pose a risk assessment challenge because their exposures are seldom documented. They follow crops, encounter sequential exposures, and often have their families with them. Although 40% to 50% of all farm workers met the migrant definition, only 19% were follow-the-crop migrants.115

Secondhand exposure occurs: In North Carolina, pesticides were found in 39 of 41 households (95%), on toys in 71%, and on children's hands in 55%.116 In a study of 213 farm workers in Washington communities and labor camps, 20% identified mixing, loading, or spraying activities. However, take-home pesticide levels and children's urinary pesticide levels were higher for those who thinned crops than for those who sprayed them.117

Urban Poor

Many factors affect the health and well-being of people living in cities, particularly minority and low-income families, including housing age and quality; poverty, crime, and nutrition status; household pesticides;35 lack of exercise resulting from unsafe neighborhoods and low walkability;118 and a disconnect among planning, public health, biology, and social factors.119 A college education is strongly associated with high self-assessment of health.120 The stresses of drugs, crime, and unemployment create a toxic environment that compounds exposure to indoor and outdoor pollutants.

In the United States, approximately 6 million children are urban poor.121 In 2 Chicago inner-city neighborhoods, living in dwellings built before 1919 was associated with child blood lead levels of more than 10 micrograms per deciliter.63 Baxter et al.122 implicated high-density, multiunit buildings as a risk factor for exposure to nitrogen dioxide and particles less than 2.5 micrometers in diameter. Air pollution studies comparing neighborhoods123 or cities124 have shown substantial intra- and intercity variability in space and time attributable partly to highways and industries.

The emphasis on asthma in children obscures the high rates of asthma in adults. A sample of central Harlem adults found that 14% reported asthma, with women being twice as likely to have activity restrictions and to report multiple emergency room visits.125 Residents from households earning less than $9000 per year were more likely to report asthma than were those from households earning more than $20 000.

Pesticides are not confined to agricultural areas or suburban lawns. Kings County (Brooklyn) and Manhattan were the 2 New York counties with the highest rate of legal pesticide application,35 mainly to control fleas and cockroaches. Pregnant women (68% Dominican, 31% Black) in northern Manhattan and South Bronx were surveyed for pesticide use and exposure; pesticide use in the home was reported by 61% of the women, and chlorpyrifos and diazinon were detected in virtually all household and personal air monitors.126 Before the chlorpyrifos ban in 2001, birth weight and height decreased by 67 grams and 0.43 centimeters for every log unit increase in cord plasma level.127 Urban gardening and locally grown food can be an important exposure pathway for metals and semivolatile organic chemicals from the atmosphere.99

Cultural Uses of Mercury

All forms of mercury are toxic, hence its widespread use in a variety of biocides. Elemental mercury (quicksilver) has been imbued with magical powers for centuries, and today many cultures covet mercury, including people in India, the Andes, and US cities. In the United States, cultural practices involving mercury are prominent in Latino Caribbean communities (Cuban, Dominican, Puerto Rican), in which mercury (called azogue or vidajan) is sold in specialty shops called botanicas. The cultural or spiritual practices in which mercury may be involved are Santeria (African Latino), Palo Mayombé (Caribbean), Candomblé (African Brazilian), Voodoo (Haitan), Espiritismo (Puerto Rican), and Parad-Shivling (Hindu). Superstitious practices are more prominent than spiritual practices. Girls carry amulets containing liquid mercury to bring good luck or attract lovers; boys carry mercury to attract money.128 Mercury droplets may be applied directly to the body, dispersed in cologne, or sprinkled around new cars or new apartments or over babies to ward off evil spirits. In rare cases, mercury may be injected, usually with severe consequences.129 The popular press has attributed the superstitious uses to advice from Santeros, but practitioners have consistently denied that they recommend mixing mercury with perfume or bath water or sprinkling it over candles or babies.40 Swallowing liquid mercury in capsules is still used as an alternative practice to relieve gastrointestinal symptoms,130 mainly in Latino and Caribbean communities; this exposure pathway is less important exposure because elemental mercury is poorly absorbed from the gastrointestinal tract.131 A cluster of children exposed to mercury brought home in amulets had elevated mercury levels, with a maximum of 1213 micrograms per liter compared with an upper limit of normal of 50 micrograms per liter.132

These cultural uses of mercury can be widespread,133 and they provide a unique exposure pathway that has been resistant to intervention. Once a home is contaminated with mercury droplets, subsequent occupants may experience exposure. The EPA134 has had more interest in cultural uses of mercury than have consumer product agencies,135 which have been reluctant to regulate mercury for fear of driving it further underground.131 Cultural uses raise controversy not only about freedom of religion, but also about blaming individuals for environmental contamination with mercury while much larger sources of contamination, such as coal-fired power plants, are weakly regulated.136 Airborne mercury released by poorly regulated Midwestern power plants is deposited all over the northeastern United States, adding to the burden of otherwise environmentally stressed communities.

RECOMENDATIONS AND CONCLUSIONS

The presence of exposure outliers in a wide variety of populations and the intersection of risk factors are important aspects of risk assessment. The same individual may be an outlier for several risk factors at once, putting his or her combined exposure and risk far above that of any modeled estimate. On the one hand, critics of risk assessment decry reliance on unrealistic default values, and on the other hand, current methodology overlooks outlier individuals facing multiple environmental and social stressors. Although various EPA guidance manuals137138 have clearly described the general concepts of exposure assessment and provided guidance on conducting an exposure assessment for unique and highly exposed populations, we strongly encourage the systematic consideration of uniquely exposed populations in all risk assessments to support decision-making at the EPA and other agencies. We advance a framework to ensure that exposure assessments consistently examine unique exposure pathways. Combining this framework with information on types of uniquely exposed populations will enhance risk assessors’ capacity to identify those who may experience high-end–exposures to environmental contaminants. The people who are often dismissed as outliers are those who are most at risk and most in need of protection. We provided scientific evidence that uniquely exposed populations with high-end-exposed individuals need to be specifically examined in risk assessments. These data should be translated into guidelines for risk assessors. The impact is greater in populations that experience multiple stressors, including multiple environmental exposures coupled with inadequate nutrition, poor access to health information and treatment, and socioeconomic stress.

We showed that data on uniquely exposed populations are often lacking or submerged in means and medians. We recommend investing in systematic data collection and reporting to fill these gaps, using complete distributional data that clearly identify high-end and high-risk individuals. These individuals are particularly likely to be found in environmental justice populations who face an excess of both environmental and socioeconomic stressors.

We suggest these approaches to research on highly exposed environmental justice communities:

  • Expand the National Health and Nutrition Examination Survey model, and expand its use to local levels, modeled on the New York City Health and Nutrition Examination Survey.139 Include questions regarding environmental justice communities, with more details on fish consumption, traditional medicines, and cosmetic use and more detailed links to demographic and geographic data on the built environment.

  • Develop detailed site-specific consumption information to assess exposure at and beyond the 95th percentile, by publishing or making available raw data from which complete distributional details can be obtained.

  • Develop a standardized methodology for assessing exposure at different distances from point-source pollution in minority, low-income, and Native American populations.

  • For studies that rely on means, encourage publication of both arithmetic and geometric means (which down-weight the right tail of distributions).

Other approaches to research will take longer to develop and execute, including determining temporal effects of contaminants on fetal development in highly exposed populations, modeling the multiple exposures that environmental justice communities face, and developing a national exposure database for high-end exposures for known high-risk populations.140,141 Risk assessment focuses on exposures averaged over time, whereas intermittent peak exposures may convey the greatest risk. An emphasis on tracking vulnerable groups is needed. Minority and low-income groups have higher residential mobility than Whites, partly because of lack of available jobs.142 Studies that emphasize tracking and follow-up will gain considerable power in detecting risk-factor interactions on exposure.

The EPA should ensure that data collected on American Indians and other groups are not collapsed into an “other” category.143 Data should be presented by tribe whenever possible. These data suggest a need to develop a holistic approach to exposure assessment for ethnic–racial, low-income, and other environmental justice communities, including broadening exposure to include religious, cultural, and other lifestyles that may not be mainstream.

Acknowledgments

We were partially funded by the Environmental Protection Agency (GS-00F-0001S), the Consortium for Risk Evaluation With Stakeholder Participation through the Department of Energy (DE-FC01-06EW07053), the National Institute of Environmental Health Sciences (P30ES005022), and the Environmental and Occupational Health Sciences Institute.

We particularly thank M. Callahan and O. Nweke for organizing the Environmental Protection Agency conference and for critically reading the article. We also thank M. Greenberg, C. W. Powers, and C. Chess for helpful information and discussions about environmental justice communities, Native Americans, and the complexities of environmental evaluation in relation to exposure, resource use, and future land use.

Note. The conclusions and interpretations reported herein are the sole responsibility of the authors and should not in any way be interpreted as representing the views of the funding agencies.

Human Participant Protection

This article is a review of other articles; thus, no human participants were used and institutional review board approval was not needed.

References

  • 1.US Environmental Protection Agency Sociodemographic Data Used or Identifying Potentially Highly Exposed Populations. Washington, DC: US Environmental Protection Agency; 1999 [Google Scholar]
  • 2.National Research Council Science and Decisions: Advancing Risk Assessment. Washington, DC: National Academies Press; 2009 [PubMed] [Google Scholar]
  • 3.National Research Council Risk Assessment in the Federal Government, Managing the Process. Washington, DC: National Academies Press; 1983 [PubMed] [Google Scholar]
  • 4.National Research Council Pesticides in the Diets of Infants and Children. Washington, DC: National Academies Press; 1993 [PubMed] [Google Scholar]
  • 5.Gochfeld M, Burger J. Environmental and ecological risk assessment. : Wallace RB, Kohatsu N, Maxey-Rosenau-Last Public Health and Preventive Medicine. 15th ed New York: McGraw-Hill, 2008:545–562 [Google Scholar]
  • 6.Weiss B, Cory-Slechta D, Gilbert SG, et al. The new tapestry of risk assessment. Neurotoxicology. 2008;29(5):883–890 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 7.Healton C, Nelson K. Reversal of misfortune: viewing tobacco as a social justice issue. Am J Public Health. 2004;94(2):186–191 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 8.Miller JE. The effects of race/ethnicity and income on early childhood asthma prevalence and health care use. Am J Public Health. 2000;90:428–430 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 9.Delfino RJ, Gong H, Linn WS, Hu Y, Pellizzari ED. Respiratory symptoms and peak expiratory flow in children with asthma in relation to volatile organic compounds in exhaled breath and ambient air. J Expo Anal Environ Epidemiol. 2003;13(5):348–363 [DOI] [PubMed] [Google Scholar]
  • 10.Institute of Medicine Unequal Treatment: Confronting Racial and Ethnic Disparities in Health Care. Washington, DC: National Academies Press; 2003 [PubMed] [Google Scholar]
  • 11.President's Cancer Panel Facing Cancer in Indian Country: the Yakama Nation and Pacific Northwest Tribes. Bethesda, MD: National Cancer Institute; 2003 [Google Scholar]
  • 12.Katz RJ. Addressing the health care needs of American Indians and Alaska Natives. Am J Public Health. 2004;94(1):13–14 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 13.Beetstra S, Derksen D, Ro M, Powell W, Fry DE, Kaufman AA. “Health commons” approach to oral health for low-income populations in a rural state. Am J Public Health. 2002;92(1):12–13 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 14.Cornelius LJ, Smith PL, Simpson GM. What factors hinder women of color from obtaining preventive health care. Am J Public Health. 2002;92(4):535–538 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 15.Gwynn RC, Thurston GD. The burden of air pollution: impacts among racial minorities. Environ Health Perspect. 2001;109(suppl 4):501–506 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 16.Gochfeld M. Occupational medicine practice in the United States since the Industrial Revolution. J Occup Environ Med. 2005;47(2):115–131 [DOI] [PubMed] [Google Scholar]
  • 17.Coronado GD, Vigoren EM, Thompson B, Griffith WC, Faustman EM. Organophosphate pesticide exposure and work in pome fruit: evidence for the take-home pesticide pathway. Environ Health Perspect. 2006;114(7):999–1006 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 18.Plog BA, Quinlan P. Fundamentals of Industrial Hygiene. 5th ed. Washington, DC: National Safety Council; 2002 [Google Scholar]
  • 19.American Lung Association Fact Sheet: Smoking and African-Americans. New York, NY: American Lung Association; 2008 [Google Scholar]
  • 20.John R, Cheney MK, Azad MR. Point-of-sale marketing of tobacco products: taking advantage of the socially disadvantaged? J Health Care Poor Underserved. 2009;20(2):489–506 [DOI] [PubMed] [Google Scholar]
  • 21.American Lung Association. Fact Sheet: Smoking and Hispanics. New York, NY: American Lung Association; 2008 [Google Scholar]
  • 22.Needham LL, Sexton K. Assessing children's exposure to hazardous environmental chemicals: an overview of selected research challenges and complexities. J Expo Anal Environ Epidemiol. 2000;10(6, pt 2):611–629 [DOI] [PubMed] [Google Scholar]
  • 23.Shalat SL, Donnelly KC, Freeman NCG, et al. Nondietary ingestion of pesticides by children in an agricultural community on the US/Mexico border: preliminary results. J Expo Anal Environ Epidemiol. 2003;13(1):42–50 [DOI] [PubMed] [Google Scholar]
  • 24.Eskenazi B, Bradman A, Castorina R. Exposures of children to organophosphate pesticides and their potential adverse health effects. Environ Health Perspect. 1999;107(suppl 3):991–1000 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 25.Coble J, Hoppin JA, Engel L, et al. Prevalence of exposure to solvents, metals, grain dust, and other hazards among farmers in the agricultural health study. J Expo Anal Environ Epidemiol. 2002;12(6):418–426 [DOI] [PubMed] [Google Scholar]
  • 26.Bradman A, Whitaker D, Quiros L, et al. Pesticides and their metabolites in the homes and urine of farmworker children living in the Salinas Valley, CA. J Expo Sci Environ Epidemiol. 2007;17(4):331–349 [DOI] [PubMed] [Google Scholar]
  • 27.Melman ST, Nimeh JW, Anbar RD. Prevalence of elevated blood lead levels in an inner-city pediatric clinic population. Environ Health Perspect. 1998;106(10):655–657 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 28.Freudenberg N. Time for a national agenda to improve the health of urban populations. Am J Public Health. 2000;90(6):837–840 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 29.Saksena S, Singh PB, Prasad RK, et al. Exposure of infants to outdoor and indoor air pollution in low-income urban areas—a case study of Delhi. J Expo Anal Environ Epidemiol. 2003;13(3):219–230 [DOI] [PubMed] [Google Scholar]
  • 30.Hysong TA, Burgess JL, Cebrian Garcia ME, O'Rourke MK. House dust and inorganic urinary arsenic in two Arizona mining towns. J Expo Anal Environ Epidemiol. 2003;13(3):211–218 [DOI] [PubMed] [Google Scholar]
  • 31.McElroy JA, Gangnon RE, Newcomb PA, et al. Risk of breast cancer for women living in rural areas from adult exposure to atrazine from well water in Wisconsin. J Expo Sci Environ Epidemiol. 2007;17(2):207–214 [DOI] [PubMed] [Google Scholar]
  • 32.Cox LH. Protecting confidentiality in small population health and environmental statistics. Stat Med. 1996;15(17–18):1895–1905 [DOI] [PubMed] [Google Scholar]
  • 33.Burger J, Gochfeld M, Jeitner C, et al. Mercury levels and potential risk from subsistence foods from the Aleutians. Sci Total Environ. 2007;384(1–3):93–105 [DOI] [PubMed] [Google Scholar]
  • 34.Landrigan PJ, Kimmel CA, Correa A, Eskenazi B. Children's health and the environment: public health issues and challenges for risk assessment. Environ Health Perspect. 2004;112(2):257–265 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 35.Landrigan PJ, Claudio L, Markowitz SB, et al. Pesticides and inner-city children: exposures, risks, and prevention. Environ Health Perspect. 1999;107(suppl 3):431–437 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 36.Columbia River Inter-Tribal Fish Commission A Fish Consumption Survey of the Umatilla, Nez Perce, Yakama, and Warm Springs Tribes of the Columbia River Basin. Portland, OR: Columbia River Inter-tribal Fish Commission; 1994. Technical rep. 94-3 [Google Scholar]
  • 37.Harris SG, Harper BL. A Native American exposure scenario. Risk Anal. 1997;17(6):789–795 [DOI] [PubMed] [Google Scholar]
  • 38.Bradman AS, Schwartz JM, Fenster L, Barr DB, Holland NT, Eskenazi B. Factors predicting organochlorine pesticide levels in pregnant Latina women living in a United States agricultural area. J Expo Sci Environ Epidemiol. 2007;17(4):388–399 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 39.Eskenazi B, Marks AR, Bradman A, et al. Organophosphate pesticide exposure and neurodevelopment in young Mexican-American children. Environ Health Perspect. 2007;115(5):792–808 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 40.Alison Newby C, Riley DM, Leal-Almeraz TO. Mercury use and exposure among Santeria practitioners: religious versus folk practice in Northern New Jersey, USA. Ethn Health. 2006;11(3):287–306 [DOI] [PubMed] [Google Scholar]
  • 41.Donatuto J, Harper BL. Issues in evaluating fish consumption rates for Native American tribes. Risk Anal. 2008;28(6):1497–1505 [DOI] [PubMed] [Google Scholar]
  • 42.Garetano G, Stern AH, Robson M, Gochfeld M. Mercury vapor in residential building common areas in communities where mercury is used for cultural purposes versus a reference community. Sci Total Environ. 2008;397(1–3):131–139 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 43.Evans GW, Kantrowitz E. Socioeconomic status and health: the potential role of environmental risk exposure. Annu Rev Public Health. 2002;23:303–331 [DOI] [PubMed] [Google Scholar]
  • 44.National Research Council Pesticides in the Diets of Infants and Children. Washington, DC: National Academies Press; 1993 [PubMed] [Google Scholar]
  • 45.Moore CF. Children and Pollution: Why Scientists Disagree. New York: Oxford University Press; 2009 [Google Scholar]
  • 46.Simon DL, Maynard EJ, Thomas KD. Living in a sea of lead—changes in blood- and hand-lead of infants living near a smelter. J Expo Sci Environ Epidemiol. 2007;17(3):248–259 [DOI] [PubMed] [Google Scholar]
  • 47.Murgueytio AM, Evans RG, Roberts D. Relationship between soil and dust lead in a lead mining area and blood lead levels. J Expo Anal Environ Epidemiol. 1998;8(2):173–186 [PubMed] [Google Scholar]
  • 48.Binder S, Sokal D, Maughan D. Estimating the amount of soil ingested by young children through tracer elements. Arch Environ Health. 1986;41(6):331–345 [DOI] [PubMed] [Google Scholar]
  • 49.Calabrese EJ, Stanek EJ, 3rd, Pekow P, Barnes RM. Soil ingestion estimates for children residing on a Superfund site. Ecotoxicol Environ Saf. 1997;36(3):258–268 [DOI] [PubMed] [Google Scholar]
  • 50.Khoury GA, Diamond GL. Risks to children from exposure to lead in air during remedial or removal activities at Superfund sites: a case study of the RSR lead smelter Superfund site. J Expo Anal Environ Epidemiol. 2003;13(1):51–65 [DOI] [PubMed] [Google Scholar]
  • 51.Reed KJ, Jimenez M, Freeman NC, Lioy PJ. Quantification of children's hand and mouthing activities through a videotaping methodology. J Expo Anal Environ Epidemiol. 1999;9(5):513–520 [DOI] [PubMed] [Google Scholar]
  • 52.Black K, Shalat SL, Freeman NCG, Jimenez M, Donnelly KC, Calvin JA. Children's mouthing and food-handling behavior in an agricultural community on the US/Mexican border. J Expo Anal Environ Epidemiol. 2005;15(3):244–251 [DOI] [PubMed] [Google Scholar]
  • 53.Freeman NCG, Ettinger A, Berry M, Rhoades G. Hygiene- and food-related behaviors associated with blood lead levels of young children from lead-contaminated homes. J Expo Anal Environ Epidemiol. 1997;7(1):103–118 [PubMed] [Google Scholar]
  • 54.Kimbrough RD, Falk H, Stehr P, Fries G. Health implications of 2,3,7,8-tetrachloro-dibenzodioxin (TCDD) contamination of residual soil. J Toxicol Environ Health. 1984;14(1):47–93 [DOI] [PubMed] [Google Scholar]
  • 55.Calabrese EJ, Stanek EJ, 3rd, Gilbert CE. Evidence of soil-pica behavior and quantification of soil ingested. Hum Exp Toxicol. 1991;10(4):245–249 [DOI] [PubMed] [Google Scholar]
  • 56.Bellinger DC, Bellinger AM. Childhood lead poisoning: the torturous path from science to policy. J Clin Invest. 2006;116(4):853–857 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 57.Annest JL, Pirkle JL, Makuc D, Neese JW, Bayse DD, Kovar MG. Chronological trend in blood lead levels between 1976 and 1980. N Engl J Med. 1983;308(23):1373–1377 [DOI] [PubMed] [Google Scholar]
  • 58.Centers for Disease Control and Prevention Preventing Lead Poisoning in Young Children. Atlanta, GA: Centers for Disease Control and Prevention; 2005 [Google Scholar]
  • 59.Needleman HL, Landrigan PJ. What level of lead in blood is toxic for children. Am J Public Health. 2004;94(1):8. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 60.Brown MJ, Meehan PJ. Health effects of blood lead levels lower than 10 ug/dl in children. Am J Public Health. 2004;94(1):8–9 [PMC free article] [PubMed] [Google Scholar]
  • 61.Miranda ML, Kim D, Galeano MAO, Paul CJ, Hull AP, Morgan SP. The relationship between early childhood blood lead levels and performance on end-of-grade tests. Environ Health Perspect. 2007;115(8):1242–1247 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 62.Jusko TA, Henderson CRJ, Lanphear BP, Cory-Slechta DA, Parsons PJ, Canfield RL. Blood lead concentrations < 10 μg/dL and child intelligence at 6 years of age. Environ Health Perspect. 2008;116(2):243–248 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 63.Dignam TA, Evens A, Eduardo E, et al. High-intensity targeted screening for elevated blood lead levels among children in 2 inner-city Chicago communities. Am J Public Health. 2004;94(11):1945–1951 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 64.Lanphear BP, Weitzman M, Eberly S. Racial differences in urban children's environmental exposures to lead. Am J Public Health. 1996;86(10):1460–1463 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 65.Pirkle JL, Kaufmann RB, Brody DJ, Hickman T, Gunter EW, Paschal DC. Exposure of the U.S. population to lead, 1991-1994. Environ Health Perspect. 1998;106(11):745–750 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 66.Lanphear BP, Hornung R, Ho M, Howard CR, Eberly S, Knauf K. Environmental lead exposure during early childhood. J Pediatr. 2002;140(1):40–47 [DOI] [PubMed] [Google Scholar]
  • 67.Tehranifar P, Leighton J, Auchincloss AH, et al. Immigration and risk of childhood lead poisoning: findings from a case-control study of New York City children. Am J Public Health. 2008;98(1):92–97 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 68.Edwards M, Triantafyllidou S, Best D. Elevated blood lead in young children due to lead-contaminated drinking water: Washington, DC, 2001–2004. Environ Sci Technol. 2009;43(5):1618–1623 [DOI] [PubMed] [Google Scholar]
  • 69.Ridolfi J. Yakama Nation Exposure Scenario for Hanford Site risk assessment. Richland, WA: Yakama Nation; 2007 [Google Scholar]
  • 70.Confederated Tribes of the Umatilla Indian Reservation Exposure Scenario for CTUIR Traditional Subsistence Lifeways. Pendleton, OR: Confederated Tribes of the Umatilla Indian Reservation; 2004 [Google Scholar]
  • 71.Harris SG. Application of the CTUIR Traditional Lifeways Exposure Scenario in Hanford Risk Assessments. Pendleton, OR: Confederated Tribes of the Umatilla Indian Reservation; 2008 [Google Scholar]
  • 72.Harper BL, Harding AD, Waterhous T, Harris SG. Traditional Tribal Subsistence Exposure Scenario and Risk Assessment Guidance Manual. Corvallis: Oregon State University Printing and Mailing; 2007. Report of grant no. EPA-STAR-J1-R831-46 [Google Scholar]
  • 73.Burger J, Gochfeld M, Pletnikoff K, Snigaroff R, Snigaroff D, Stamm T. Ecocultural attributes: evaluating ecological degradation in terms of ecological goods and services versus subsistence and tribal values. Risk Anal. 2008;28(5):1261–1271 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 74.Burger J. American Indians, hunting and fishing rates, risk, and the Idaho National Engineering and Environmental Laboratory. Environ Res. 1999;80(4):317–329 [DOI] [PubMed] [Google Scholar]
  • 75.Harper BL, Harris SG. A possible approach for setting a mercury risk-based action level based on tribal fish ingestion rates. Environ Res. 2008;107(1):60–68 [DOI] [PubMed] [Google Scholar]
  • 76.Richardson GM, Currie DJ. Estimating fish consumption rates for Ontario Amerindians. J Expo Anal Environ Epidemiol. 1993;3(1):23–38 [PubMed] [Google Scholar]
  • 77.DeWeese AD, Kmiecik NE, Chiriboga ED, Foran JA. Efficacy of risk-based, culturally sensitive Ogaa (Walleye) consumption advice for Anishinaabe tribal members in the Great Lakes region. Risk Anal. 2009;29(5):729–742 [DOI] [PubMed] [Google Scholar]
  • 78.Muckle G, Ayotte P, Dewailly E, Jacobson SW, Jacobson JL. Determinants of polychlorinated biphenyls and methylmercury exposure in Inuit women of childbearing age. Environ Health Perspect. 2001;109(9):957–963 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 79.Berti PR, Receveur O, Chan HM, Kuhnlein HV. Dietary exposure to chemical contaminants from traditional food among adult Dene/Metis in the Western Northwest Territories, Canada. Environ Res. 1998;76(2):131–142 [DOI] [PubMed] [Google Scholar]
  • 80.US Environmental Protection Agency Fact Sheet: National Listing of Fish and Wildlife Advisories. Washington, DC: US Environmental Protection Agency; 2001. Report no. EPA-823-F-01-010 [Google Scholar]
  • 81.West P, Fly J, Larkin F, Marans P. Minority anglers and toxic fish consumption: evidence of the state-wide survey of Michigan. Bryant B, Mohai P, Race and the Incidence of Environmental Hazards. Boulder, CO: Westview Press; 1990:100–113 [Google Scholar]
  • 82.Toy KA, Polissar NL, Liao S, Mittelstaedt GD. A Fish Consumption Study of the Tulalip and Squaxin Island Tribes of the Puget Sound Region. Marysville, WA: Tulalip Tribes, Department of the Environment; 1996 [Google Scholar]
  • 83.Walker DE, Pritchard LW. Estimated Radiation Doses to Yakama Tribal Fisherman. Boulder, CO: Walker Research Group; 1999 [Google Scholar]
  • 84.Burger J. Consumption patterns and why people fish. Environ Res. 2002;90(2):125–135 [DOI] [PubMed] [Google Scholar]
  • 85.Burger J. Daily consumption of wild fish and game: exposures of high end recreationists. Int J Environ Health Res. 2002;12(4):343–354 [DOI] [PubMed] [Google Scholar]
  • 86.Ebert ES, Harrington NW, Boyle KJ, Knight JW, Keenan RE. Estimating consumption of freshwater fish among Maine anglers. N A J Fish Manag. 1993; 13(4):737–745 [Google Scholar]
  • 87.Connelly NA, Knuth BA, Brown TL. Sportfish consumption patterns of Lake Ontario anglers and the relationship of health advisories. N A J Fish Manage. 1996;16(1):90–101 [Google Scholar]
  • 88.Jacobs HL, Kahn HD, Stralka KA, Phan DB. Estimates per capita fish consumption in the US based on the continuing survey of food intake by individuals. Risk Anal. 1998;18(3):283–291 [DOI] [PubMed] [Google Scholar]
  • 89.Anderson AC, Rice JC. Survey of fish and shellfish consumption by residents of the greater New Orleans area. Bull Environ Contam Toxicol. 1993;51(4):508–514 [DOI] [PubMed] [Google Scholar]
  • 90.Williams RL, O'Leary JT, Sheaffer AL, Mason D. An Examination of Fish Consumption by Indiana Recreational Anglers: An On-Site Survey. West Lafayette, IN: Purdue University; 2000. Technical rep. 99-D-HDFW-2 [Google Scholar]
  • 91.Murray DM, Burmaster DE. Estimated distribution for average daily consumption of total and self-caught fish for adults in Michigan angler households. Risk Anal. 1994;14(4):513–519 [Google Scholar]
  • 92.Stern AH, Korn LR, Ruppel BE. Estimation on fish consumption and methylmercury intake in the New Jersey population. J Expo Anal Environ Epidemiol. 1996;6(4):503–527 [PubMed] [Google Scholar]
  • 93.May H, Burger J. Fishing a polluted estuary: risk and risk perception of recreational fishermen. Risk Anal. 1996;16(4):459–471 [DOI] [PubMed] [Google Scholar]
  • 94.Mayfield DB, Robinson S, Simmonds J. Survey of fish consumption patterns of King County (Washington) recreational anglers. J Expo Sci Environ Epidemiol. 2007;17:604–612 [DOI] [PubMed] [Google Scholar]
  • 95.Moya J. Overview of fish consumption rates in the United States. Human Ecol Risk Assess. 2004;10(6):1195–1211 [Google Scholar]
  • 96.Burger J, Gaines KF, Lord CG, Brisbin IL, Shukla S, Gochfeld M. Metal levels in raccoon tissues: differences on and off the Department of Energy's Savannah River site in South Carolina. Environ Monit Assess. 2002;74(1):67–84 [DOI] [PubMed] [Google Scholar]
  • 97.Sechena R, Liao S, Lorenzana R, Nakano C, Polissar N, Fenske R. Asian American and Pacific Islander seafood consumption—a community-based study in King County, Washington. J Expo Anal Environ Epidemiol. 2003; 13(4):256–266 [DOI] [PubMed] [Google Scholar]
  • 98.Ingram DD, Makuc DM, Eberhardt MS. Health, United States, 2001. With Urban and Rural Health Chartbook. Hyattsville, MD: National Center for Health Statistics; 2001 [Google Scholar]
  • 99.Hartley D. Rural health disparities, population health, and rural culture. Am J Public Health. 2004;94(10):1675–1678 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 100.Lobscheid AB, Maddalena RL, McKone TE. Contribution of locally grown foods in cumulative exposure assessment. J Expo Anal Environ Epidemiol. 2004;14(1):60–73 [DOI] [PubMed] [Google Scholar]
  • 101.Sullivan PA. Vermiculite, respiratory disease and asbestos exposure in Libby, Montana: update of a cohort mortality study. Environ Health Perspect. 2007;115(4):579–585 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 102.Probst JC, Moore CG, Glover SH, Samuels ME. Person and place: the compounding effects of race/ethnicity and rurality on health. Am J Public Health. 2004;94(10):1695–1703 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 103.Eberhardt MS, Pamuk ER. The importance of place of residence: examining health in rural and nonrural areas. Am J Public Health. 2004;94(10):1682–1686 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 104.Fall JA, Stanek RT, Brown L, Utermohle C. The Harvest and Use of Fish, Wildlife and Plant Resources in False Pass, Unimak Island, Alaska. Juneau, AK; Alaska Department of Fish and Game, Division of Subsistence, 2006. Tech. rep. 183 [Google Scholar]
  • 105.Hamrick K, Smith J. Final Report: Subsistence Food Use in Unalaska and Nikolski for Aleutian/Probilof Island. Anchorage, AK: Association Institute for Circumpolar Health Studies, University of Alaska-Anchorage; 2003 [Google Scholar]
  • 106.Strong LL, Thompson B, Koepsell TD, Meischke H, Coronado GD. Reducing the take-home pathway of pesticide exposure: behavioral outcomes from the Para Ninos Saludables study. J Occup Environ Med. 2009;51(8):922–933 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 107.McCauley LA, Anger WK, Keifer M, Langley R, Robson MG, Rohlman D. Studying health outcomes in farmworker populations exposed to pesticides. Environ Health Perspect. 2006;114(6):953–960 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 108.Quandt SA, Hernandez-Valero MA, Grzywacz JG, Hovey JD, Gonzales M, Arcury TA. Workplace, household, and personal predictors of pesticide exposure for farmworkers. Environ Health Perspect. 2006;114(6):943–952 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 109.Strong LL, Thompson B, Coronado GD, Griffith WC, Vigoren EM, Islas I. Health symptoms and exposure to organophosphate pesticides in farmworkers. Am J Ind Med. 2004;46(6):599–606 [DOI] [PubMed] [Google Scholar]
  • 110.Ward MH, Lubin J, Giglierano J, et al. Proximity to crops and residential exposure to agricultural herbicides in Iowa. Environ Health Perspect. 2006;114(6):893–897 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 111.Roberts EM, English PB, Grether JK, Windham GC, Somberg L, Wolff C. Maternal residence near agricultural pesticide applications and autism spectrum disorders among children in California Central Valley. Environ Health Perspect. 2007;115(10):1482–1489 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 112.Thompson B, Coronado GD, Grossman JE, et al. Pesticide take-home pathway among children of agricultural workers: study design, methods, and baseline findings. J Occup Environ Med. 2003;45(1):42–53 [DOI] [PubMed] [Google Scholar]
  • 113.Vaughan E. Chronic exposure to an environmental hazard: risk perceptions and self-protective behavior. Health Psychol. 1993;12(1):74–85 [DOI] [PubMed] [Google Scholar]
  • 114.Mirabelli MC, Wing S. Proximity to pulp and paper mills and wheezing symptoms among adolescents in North Carolina. Environ Res. 2006;102(1):96–100 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 115.National Agricultural Workers Survey. Available at: http://www.doleta.gov/agworker/naws.cfm. Published 2005. Updated January 5, 2011. Accessed August 19, 2010.
  • 116.Arcury TA, Grzywacz JG, Davis SW, Barr DB, Quandt SA. Organophosphorus pesticide urinary metabolite levels of children in farmworker households in eastern North Carolina. Am J Ind Med. 2006;49(9):751–760 [DOI] [PubMed] [Google Scholar]
  • 117.Coronado GD, Thompson B, Strong L, Griffith WC, Islas I. Agricultural task and exposure to organophosphate pesticides among farmworkers. Environ Health Perspect. 2004;112(2):142–147 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 118.Greenberg MR, Renne J. Where does walkability matter the most? An environmental justice interpretation of New Jersey data. J Urban Health. 2005;82(1):90–100 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 119.Corburn J. Confronting the challenges in reconnecting urban planning and public health. Am J Public Health. 2004(4);94:541–564 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 120.Ettner SL, Grzywacz JG. Socioeconomic status and health among Californians: an examination of multiple pathways. Am J Public Health. 2003;93(3):441–444 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 121.Dalaker J, Naifeh M. Poverty in the United States: 1997. Washington, DC: US Census Bureau; 1998 [Google Scholar]
  • 122.Baxter LK, Clougherty JE, Laden F, Levy JI. Predictors of concentrations of nitrogen dioxide, fine particulate matter, and particle constituents inside of lower socioeconomic status urban homes. J Expo Sci Environ Epidemiol. 2007;17(5):433–444 [DOI] [PubMed] [Google Scholar]
  • 123.Keeler GJ, Dvonch JT, Yip FY, et al. Assessment of personal and community-level exposure to particulate matter among children with asthma in Detroit, Michigan as part of Community Action Against Asthma (CAAA). Environ Health Perspect. 2002;110(suppl 2):173–181 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 124.Dockery DW, Pope CA, 3rd, Xu X, et al. An association between air pollution and mortality in six U.S. cities. N Engl J Med. 1993;329(24):1753–1759 [DOI] [PubMed] [Google Scholar]
  • 125.Northridge ME, Meyer IH, Dunn L. Overlooked and underserved in Harlem: a population-based survey of adults with asthma. Environ Health Perspect. 2002;110(suppl 2):217–220 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 126.Whyatt RM, Garfinkel R, Hoepner LA, et al. Within- and between-home variability in indoor-air insecticide levels during pregnancy among an inner-city cohort from New York City. Environ Health Perspect. 2007;115(3):383–389 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 127.Whyatt RM, Camann D, Perera FP, et al. Biomarkers in assessing residential insecticide exposures during pregnancy and effects on fetal growth. Toxicol Appl Pharmacol. 2005;206(2):246–254 [DOI] [PubMed] [Google Scholar]
  • 128.Johnson C. Elemental mercury use in religious and ethnic practices in Latin American and Caribbean communities in New York City. Popul Environ. 1999;20(5):443–453 [Google Scholar]
  • 129.Prasad VL. Subcutaneous injection of mercury: “warding off evil.” Environ Health Perspect. 2004;112(13):1326–1328 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 130.Geffner ME, Sandler A. Oral metallic mercury: a folk remedy for gastroenteritis. Clin Pediatr (Phila). 1980;19(6):435–437 [DOI] [PubMed] [Google Scholar]
  • 131.New Jersey Department Environmental Protection Report of the Mercury Task Force. Trenton, NJ: New Jersey Department Environmental Protection; 2001, Vol. 1 [Google Scholar]
  • 132.Forman J, Moline J, Cernichiari E, et al. A cluster of pediatric metallic mercury exposure cases treated with meso-2,3-dimercaptosuccinic acid (DMSA). Environ Health Perspect. 2000;108(6):575–577 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 133.Wendroff AP. Magico-religious use in Caribbean and Latino communities: pollution, persistence, and politics. Environ Pract. 2005;7(2):87–96 [Google Scholar]
  • 134.US Environmental Protection Agency Task Force on Ritualistic Uses of Mercury Report. Washington, DC: US Environmental Protection Agency; 2004. Report no. EPA/540-R-01-005 [Google Scholar]
  • 135.Wendroff AP. Magico-religious mercury use and cultural sensitivity. Am J Public Health. 1995;85(3):409–410 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 136.Paul S. Mercury rising: for a decade researchers have suspected that a magical metal is an underground health scourge. Now a partnership of science and religion may finally tell New Yorkers the truth. City Limits. 2003;28(2):26 [Google Scholar]
  • 137.US Environmental Protection Agency Environmental Equity: Reducing the Risk for All Communities. Washington, DC: US Environmental Protection Agency; 1992. Report no. EPA230-R92-008 [Google Scholar]
  • 138.US Environmental Protection Agency Guidance for Conducting Fish and Wildlife Consumption Surveys. Washington, DC: US Environmental Protection Agency; 1998. Report no. EPA-823-B-98-007 [Google Scholar]
  • 139.New York City Health and Nutrition Examination Survey. Available at: http://www.nyc.gov/html/doh/html/hanes/hanes.shtml. Published 2010. Accessed December 4, 2010.
  • 140.Graham J, Walker KD, Berry M, et al. Role of exposure databases in risk assessment. Arch Environ Health. 1992;47(6):408–420 [DOI] [PubMed] [Google Scholar]
  • 141.Sexton K, Kleffman DE, Callahan MA. An introduction to the National Human Exposure Assessment Survey (NHEXAS) and related phase 1 field studies. J Expo Anal Environ Epidemiol. 1995;5(3):229–232 [PubMed] [Google Scholar]
  • 142.Latos CJ. Non-white migration patterns in northern metropolitan areas, 1960-1970: the interaction between economic and affinitive factors. Rev Black Polit Econ. 1984;13(3):5–19 [DOI] [PubMed] [Google Scholar]
  • 143.Burhansstipanov L, Satter DE. Office of Management and Budget racial categories and implications for American Indians and Alaska Natives. Am J Public Health. 2000;90(11):1720–1723 [DOI] [PMC free article] [PubMed] [Google Scholar]

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