Children's Exposure to Pesticides and Related Health Outcomes

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Although the use of pesticides in and around U.S. homes and on agricultural crops is common, we are just beginning to understand the potentially adverse health effects of such exposures. There is widespread concern about how exposure to pesticides might affect children, who are likely to be the most vulnerable to these effects. The NIEHS/EPA Centers for Children’s Environmental Health and Disease Prevention Research (Children’s Centers) apply community-based participatory research (CBPR) to understand the degree of children’s exposure to pesticides, potential sensitivity and genetic susceptibility of children to pesticides, and how to reduce or prevent children’s exposure to these chemicals. Pesticides - Additional Resources

Question 1 (Concerns): What are the primary concerns about pesticide exposures in children and how is EPA addressing these concerns?

Question 2 (Exposure): What are the Children’s Centers learning about children’s exposure to pesticides?

Question 3 (Susceptibility): What are the Children’s Centers learning about children’s susceptibility to pesticides?

Question 4 (Effects): What are the Children’s Centers learning about the effects of pesticides on children?

Question 5 (Prevention): What are the Children’s Centers learning about effective ways to reduce or prevent children’s exposure to pesticides in the environment?

Question 1 (Concerns): What are the primary concerns about pesticide exposures in children and how is EPA addressing these concerns?

Research has shown that children are not “little adults” – they have different exposures, different susceptibilities and sensitivities, and different outcomes when exposed to substances in the environment. Because children are still developing, the timing of an exposure to chemicals such as pesticides in terms of life stage can be critical in determining the effects. Children also are exposed differently than adults – they are closer to the ground, young children are crawlers and toddlers and tend to pick things up and put them in their mouths. In addition, children also have a higher surface to volume ratio than adults, so any exposure may affect them proportionately more.

Documented effects in children of exposure to certain pesticides include poorer growth and impact on neurodevelopment. Some groups, such as children of farmworkers, are likely to be even more vulnerable due to their higher levels of exposure to pesticides (Bradman et al 2006). To study these issues, a group of the Children’s Centers are focusing their research on the range of exposures of children to pesticides, children’s sensitivitiy and susceptibility to these compounds, the potential effects of pesticides on children and how to reduce or prevent these effects.

Types of Pesticides
There are four major types of pesticides/insecticides in wide use in the U.S.: organophosphates (OPs), organochlorines (OCs) and pyrethroids/pyrethrins.

Organophosphate (OP) Pesticides affect the nervous system by inhibiting cholinesterase (ChE) – the enzyme that regulates acetylcholine, a vital neurotransmitter. Some are very poisonous (they were used in World War II as nerve agents), however they are usually not persistent in the environment. They are used to control insect pests on a variety of food and feed crops, and millions of pounds of these chemicals are applied to agricultural crops each year. There is evidence from studies of both animals and humans that chronic low-level exposure to these chemicals may affect neurodevelopment (Rauh et al. 2006, Eskenazi et al. 2007). Research at the Children’s Centers has primarily focused on the exposure, susceptibility and effects of the OP pesticides on children’s health and how to reduce or prevent them. Examples: chlorpyrifos (more on this chemical ), parathion, diazinon.

Organochlorine (OC) Pesticides were commonly used in past years but many have now been removed from the market in the U.S. due to their health and environmental effects and their persistence in the environment (examples include DDT and chlordane).

Carbamate Pesticides: These chemicals affect the nervous system in the same way as OPs, by disrupting an enzyme that regulates acetylcholine.

Pyrethroid Pesticides were developed as a synthetic version of the naturally occurring pesticide pyrethrin found in chrysanthemums and have been modified to increase their stability in the environment. Some synthetic pyrethroids are toxic to the nervous system.

The EPA has withdrawn permission for use of a number of pesticides which have been associated with possible cancer effects, fertility problems, or developmental neurotoxicity in animal studies (Phillips 2006).

For more information, see http://www.epa.gov/pesticides/about/types.htm and http://www.epa.gov/pesticides/factsheets/.

Question 2 (Exposure): What are the Children’s Centers learning about children’s exposure to pesticides?

Children’s Center scientists have shown that blood and urine specimens from pregnant women in both urban and agricultural environments show measurable levels of pesticides, suggesting that the fetus can be exposed to these chemicals during early development (Kimmel et al. 2005; UC Berkeley Children’s Center, Castorina et al. 2003; Columbia Children’s Center, Whyatt et al. 2003);

Children in urban and rural environments are exposed to a complex mix of agricultural and household pesticides, environmental tobacco smoke, and polycyclic aromatic hydrocarbons (PAHs) and these can be combined with negative social factors that can impact their early growth and development (Kimmel et al. 2005; UC Berkeley, Eskenazi et al 2004; Columbia, Perera et al. 2004, Rauh et al. 2004; Mt. Sinai, Berkowitz et al. 2004).

Children in farmworker families may be particularly vulnerable as they are often exposed to pesticides from multiple pathways, including pesticide drift from agricultural fields, take-home exposure from their parents and breast milk from a mother who may also work or who may have worked in the fields. The UC Berkeley Children’s Center found that toddlers in farmworker communities absorb twice the amount of multiple pesticide residues on their clothing (socks and union suits) compared to younger crawling children. (UC Berkeley, Bradman et al. 2006)

A study at the University of Washington Children’s Center examined children’s exposure to OP pesticides in an agricultural community in central Washington State. Median house dust concentrations of dimethyl OP pesticides in homes of agricultural families were seven times higher than those of reference families. Median pesticide concentrations in house dust and metabolite concentrations in urine from agricultural families were significantly higher in the children living near treated orchards (within 200 ft or 60 m) than those living more distant from treated orchards. Study results indicate that children living with parents who work with agricultural pesticides, or who live in proximity to pesticide-treated farmland, have higher exposures than do other children living in the same community (Lu, Fenske et al. 2000).

Question 3 (Susceptibility): What are the Children’s Centers learning about children’s susceptibility to pesticides?

Children’s Center research has focused extensively on the area of which groups of children may be more sensitive or susceptible to pesticide effects. Results include the following:

Newborns in farmworker communities exposed to several organophosphate pesticides (OPs) display broad variability (26-fold to 160-fold) in sensitivity to OPs due to variations in a gene labeled as PON1 (paraoxonase 1). This gene codes for the paraoxonase enzymes which metabolize many OPs but the enzymes vary in both serum levels and detoxification efficiencies, depending on which version of the gene is present. This indicates a far greater variability in pesticide-detoxification capability than previously predicted (University of Washington, Furlong et al. 2005; Furlong et al. 2006; UC Berkeley, Holland et al. 2006).

To investigate individual susceptibility to pesticides, the Mount Sinai Children’s Center examined linkages of five PON single nucleotide polymorphisms (SNPs), including PON2. By combining this information with data on PON1 activity levels in maternal prenatal blood and cord blood, investigators were able to demonstrate the greater susceptibility of newborns to the effects of OP pesticides. Their PON1 activity was 1/3rd to 1/5th lower than their mothers’ levels. PON1 levels and infant-maternal activity also differed by race/ethnicity. For example, Caucasian infants with the CC promoter polymorphism in one SNP had more than 200% greater PON1 activity than those with an alternate genotype (TT). A grant from the NIEHS Environmental Genome Project has been awarded further to develop this technology (Mount Sinai, Chen et al. 2003, Chen et al. 2005).

Question 4 (Effects): What are the Children’s Centers learning about the effects of pesticides on children?

A prospective epidemiological study at the Mount Sinai Children’s Center showed that babies exposed in utero to higher levels of OP insecticides are smaller at birth. Decrements in birth weight and birth length were magnified by low maternal expression levels of the pesticide-metabolizing enzyme paraoxonase (PON1). In the same cohort, researchers found that in utero exposure to OPs and DDE (a contaminant and breakdown product of DDT ) were associated with measures of neurodevelopmental delay up to age 7. PON1 levels appear to modulate these effects (Mount Sinai, Berkowitz et al. 2004).

Prenatal exposure to pesticides was common in an urban cohort of pregnant women enrolled at the Columbia Children’s Center as a result of indoor insecticide use, where exposure to the OP pesticides chlorpyrifos and diazinon was associated with adverse birth outcomes. For instance, researchers noted average birth weight decrements of 6.6 ounces. Investigators found that after the EPA ban on these two pesticides for residential use in 2000-2001, exposure within the study population was greatly reduced and this positively impacted public health by significantly increasing healthy births, higher infant birth weights and birth lengths within a year of the regulation being implemented. (Columbia, Whyatt et al. 2004, Whyatt et al. 2005).

Urban children prenatally exposed to high levels of the OP pesticide
chlorpyrifos were significantly more likely than children exposed to low
levels of this pesticide to experience delay in both psycho-motor and
mental development at 36 months of age (Columbia, Rauh et al. 2006). In an agricultural community, increasing maternal OP metabolites in urine
during pregnancy were associated with poorer mental development at age 24 months (UC Berkeley, Eskenazi et al. 2007) In addition, highly
exposed children were significantly more likely to exhibit symptoms of
pervasive developmental disorder (Columbia, Rauh et al. 2006, UC
Berkeley, Eskenazi et al. 2007). The Columbia study also found higher
risk of ADHD and attentional disorders in children with higher OP
exposures, although the UC Berkeley study did not.

The UC Berkeley Center examined the association of maternal levels of
DDT (and its breakdown product, DDE) during pregnancy and child
neurodevelopment using the Bayley Scales of Infant Development. This
study found lower mental development index scores at 12 and 24 months of age among women with higher DDT levels during pregnancy. The effect corresponded to 7- to 10-point decreases in mental development scores across the range of DDT exposure of the population. However, even when mothers had substantial exposure, breastfeeding was usually associated positively with Bayley scale scores (UC Berkeley, Eskenazi et al 2006).

To study the long-term consequences of prenatal exposure to DDE, the Mount Sinai Children’s Center conducted a follow-up study of children born in the 1970s to mothers who had participated in the Collaborative Perinatal Project. Researchers found diminished IQ up to age 17.

Question 5 (Prevention): What are the Children’s Centers learning about effective ways to reduce or prevent children’s exposure to pesticides in the environment?

Two projects, at the Columbia and Mount Sinai children’s centers, have provided data to show that building-wide Integrated Pest Management (IPM) is cost-effective over the long term and should be implemented at the citywide or even nationwide level of public housing maintenance.

IPM is an environmentally sustainable pest control strategy that uses a variety of methods tailored to the biology and behavior of insects and rodents, including sealing of pest entry points such as cracks and crevices, and it also includes educating residents as to how to avoid attracting the pests. For IPM, pesticides are used only as a last resort, and generally only low-toxicity pesticides are used in specific areas of the dwelling where the pests are more likely to be present.

A community-based IPM intervention project in East Harlem, New York City by the Mount Sinai Children’s Center has demonstrated that (1) It is possible to reduce residential use of pesticides in the inner city and (2) showed that it is practical to introduce Integrated Pest Management (IPM) techniques on a wide scale. The Center has provided extensive community education regarding IPM to community residents through educational programs at schools and community agencies (Mount Sinai, Brenner et al. 2003).

A community-based IPM intervention project in Harlem, New York City by the Columbia Children’s center demonstrated that insect (cockroach) infestations could be significantly decreased by IPM. In the intervention group, levels of piperonyl butoxide (a pyrethroid synergist used as a test for the presence of pyrethroid insecticides) were significantly lower in indoor air samples after the intervention. Insecticides were detected in maternal blood samples collected at delivery from controls but not from the intervention group. This was the first study to use biologic dosimeters of prenatal pesticide exposure for assessing effectiveness of IPM and suggests that IPM is an effective strategy for reducing both pest infestation levels and the internal dose of insecticides during pregnancy (Columbia, Williams et al. 2006).

The Centers provided advice to the U.S. EPA leading to the Agency’s decision in 2000-2001 to ban chlorpyrifos and diazinon for residential use. These were two of the most widely used and highly toxic OP pesticides. The Columbia Children’s Center documented that exposure to children in their study population was dramatically reduced after the ban (Columbia, Whyatt et al. 2004, Whyatt et al. 2005).

Results on IPM from both the Mount Sinai and Columbia Children’s Centers have supported new proposals for community and government policy in pesticide use and regulation, and the Department of Housing in New York City used these findings as the basis for new city-wide policies to implement IPM in public housing throughout the City.

Children’s Centers Collaboration on PON1 Demonstrates Wide Range in Susceptibility to Pesticide Effects

Several of the Children’s Centers have collaborated on studies of how pesticides, specifically OPs, may impact children’s health. This collaboration has shown that there is a much wider range of susceptibility to these pesticides among both children and adults than previously thought. Although some OPs were banned in 2000-2001 for residential use in the U.S. by the EPA, mainly because of risks to children, most are still widely used in agriculture. The Centers have examined the health effects of OP pesticide exposure, how they are metabolized and how gene-environment interactions may modify health risks from these compounds.

The primary mechanism of OP toxicity is associated with inhibition of the activity of acetylcholinesterase (AChE), an enzyme necessary for the proper functioning of the nervous system because it regulates acetylcholine, a vital neurotransmitter. Recent studies have focused on paraoxonase 1 (PON1), a liver and serum enzyme that breaks down the toxic metabolites of a number of OP pesticides, including diazinon and chlorpyrifos, and its role in modulating the toxicity of OPs.

Paraoxonase takes its name from the ability to hydrolyze paraoxon (PO), the toxic metabolite of the insecticide parathion. Other OP substrates of PON1 include chlorpyrifos oxon (CPO) and diazoxon (DZO), the active metabolites of chlorpyrifos and diazinon, respectively (Costa, Cole and Furlong 2006).

PON1 Variability

The PON1 gene has several single nucleotide polymorphisms (SNPs, or genetic variations) that influence both its level of expression and its catalytic activity, thereby determining the rates at which a given individual will detoxify a specific pesticide. In other words, the form of the PON1 gene carried by an individual tells the body to make the detoxifying enzyme which can vary both its concentration in the bloodstream and its effectiveness.

The ability of the PON1 enzyme to detoxify OP pesticides is determined by whether a person has the Q or R form of the PON1 gene at position 192 on the chromosome – the amino acid at that position can either be glutamine (Q) or arginine (R). People with the QQ genotype (who have two copies of the Q form of the PON1 gene) produce a PON1 enzyme that is significantly less efficient at detoxifying chlorpyrifos. People with the RR genotype (who have two copies of the R variant of the PON1 gene) produce a PON1 enzyme that is significantly more efficient at detoxifying chlorpyrifos. Inheriting one type of gene from each parent leads to a QR genotype with intermediate detoxifying ability. Additional genetic variants also affect the serum levels of enzyme available and it is mainly the serum level of PON1 enzyme that determines detoxifying ability for diazinon.

Investigators at the UC Berkeley and University of Washington Children’s Centers have shown that the OP detoxifying ability of PON1 varies greatly among individuals. As a highly accurate way to predict the functional PON1192 genotype as well as the phenotype (the quality of the PON1 enzymes) from biological samples, researcher Clement Furlong and colleagues at the UW Children’s Center developed a two-substrate enzyme kinetic analysis. The method results in a two-dimensional plot (see below) which displays the activity levels/hydrolysis rates of diazoxonase, the form of the PON1 enzyme which detoxifies the OP pesticide diazinon, and paraoxonase, the enzyme form which detoxifies the OP pesticide parathion. This plot works because the catalytic efficiency of hydrolysis of both the Q and R forms of diazoxonase is equivalent but the R form is about twice as efficient as the Q form for paraoxonase, separating the points into three lines. The assay also provides the level of blood plasma PON1 activity. The combination of functional PON1192 genotype and plasma level is termed “PON1 status” to enable comparisons between individuals. This encompasses the PON1(192)Q/R polymorphism (which affects catalytic ability toward different substrates) and PON1 levels (which are modulated in part by a C-108T polymorphism) over straight genotyping. Note the large variability in PON1 levels, even among individuals of the same Q192R genotype. (Furlong et al. 2006, Costa et al 2006).

PON1 status plot for mothers and newborns for a subset of the CHAMACOS cohort from the UC Berkeley Children's Center as developed by the University of Washington Children's Center.

Children at increased risk of health effects from pesticides due to lower PON1 detoxifying ability

For all groups, infants are at particular risk of health effects from OP pesticides because the level of PON1 enzyme in newborns averages one-third or less than that of adults and developmental onset of PON1 is highly variable among children – it can take six months to two years for a baby to develop mature enzyme levels. PON1 levels may be even lower before birth, because premature infants have lower PON1 activity than babies carried to term (Costa et al. 2006 ). Among adults, PON1 levels can vary by 13-fold or more (Furlong et al. 2006 ). Of particular concern are exposures of pregnant mothers and newborns with low PON1 status. Low PON1 activity during early development may be involved in enhanced sensitivity of the young toward organophosphate toxicity.

Using blood samples from maternal-newborn pairs in the UC Berkeley Center's CHAMACOS cohort, investigators at the University of Washington Children’s Center found that PON1 status predicts a 65-fold to 160-fold difference in sensitivity to some OPs in the study population, with an average of 6- to 10-fold variability in sensitivity between groups of mothers and their newborns. The research demonstrates that both the quality and quantity of the PON1 enzyme is important in determining its detoxification capacity ( Furlong et al. 2006 , Holland et al. 2006 ).

Mount Sinai Center research confirms that neonates may have a lower PON1 activity level than adults, and that there are differences in PON1 activity between ethnic groups. The frequency of the PON1 genotype also varies by ethnicity. Approximately 10 to 20 percent of African Americans have the less efficient QQ genotype, compared with 50 percent of whites. Approximately 25 to 35 percent of the Latino population has the less efficient QQ genotype as well.

The Mount Sinai Children’s Center has shown further evidence of PON1 variability, demonstrating that neonates have lower PON1 activity than adults, and differences between ethnic groups. The Center has also developed new, high-throughput techniques for geno- and phenotyping of PON1 and other pesticide-metabolizing enzymes and found that decreased maternal PON1 levels are associated with a small reduction in newborn head circumference.

Certain major factors such as environmental chemicals, drugs, smoking, alcohol, diet, gender, age and disease conditions have been shown to modulate PON1 activity in either direction. As PON1 plays a protective role in OP toxicity, and because of its antioxidant capacity in cardiovascular disease, a better understanding of how PON1 can be modulated by environmental factors has potential toxicological and clinical consequences (Costa, Vitalone, Cole and Furlong 2005).

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Mount Sinai Children’s Center

University of California - Berkeley

University of Washington

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EPA provides a number of ways to learn about the effects of pesticides on human health. For more information, please visit
http://www.epa.gov/pesticides/

References

Berkowitz GS, Wetmur JG, Birman-Deych E, Obel J, Lapinski RH, Godbold JH,
Holzman IR, Wolff MS 2004. In utero pesticide exposure, maternal paraoxonase activity, and head circumference. Environ Health Perspect. 2004 Mar; 112(3):388-91.

Bradman A, Whitaker D, Quiros L, Castorina R, Henn BC, Nishioka M, Morgan J, Barr DB, Harnly M, Brisbin JA, Sheldon LS, McKone TE, Eskenazi B 2006. Pesticides and their Metabolites in the Homes and Urine of Farmworker Children Living in the Salinas Valley, CA. J Expo Sci Environ Epidemiol. 2006 May 31;

Brenner BL, Markowitz S, Rivera M, Romero H, Weeks M, Sanchez E, Deych E,
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Castorina R, Bradman A, McKone TE, Barr DB, Harnly ME, Eskenazi B 2003.
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Chen J, Chan W, Wallenstein S, Berkowitz G, Wetmur JG 2005. Haplotype-phenotype relationships of paraoxonase-1. Cancer Epidemiol Biomarkers Prev. 2005 Mar;14(3):731-4.

Chen J, Kumar M, Chan W, Berkowitz G, Wetmur JG 2003. Increased influence of genetic variation on PON1 activity in neonates. Environ Health Perspect. 2003 Aug;111(11):1403-9. Comment in: Environ Health Perspect. 2003 Aug;111(11):A591.

Costa LG, Cole TB and Furlong CE 2006. Gene-environment interactions: Paraoxonase (PON1) and Sensitivity to Organophosphate Toxicity. Lab Med. 2006;37(2):109-114.
Alternate access: http://www.medscape.com/viewarticle/522383

Costa LG, Cole TB, Vitalone A, Furlong CE 2005. Measurement of paraoxonase (PON1) status as a potential biomarker of susceptibility to organophosphate toxicity. Clin Chim Acta. 2005 Feb;352(1-2):37-47.

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Furlong CE, Holland N, Richter RJ, Bradman A, Ho A, Eskenazi B 2006.
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Holland N, Furlong C, Bastaki M, Richter R, Bradman A, Huen K, Beckman K,
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Kimmel CA, Collman GW, Fields N, Eskenazi B 2005. Lessons learned for the National Children's Study from the National Institute of Environmental Health Sciences/U.S. Environmental Protection Agency Centers for Children's Environmental Health and Disease Prevention Research. Environ Health Perspect. 2005 Oct;113(10):1414-8.

Lu C, Fenske RA, Simcox NJ, Kalman D 2000. Pesticide exposure of children in an agricultural community: evidence of household proximity to farmland and take home exposure pathways. Environ Res. 2000 Nov;84(3):290-302.

Perera FP, Rauh V, Whyatt RM, Tsai WY, Bernert JT, Tu YH, Andrews H, Ramirez J, Qu L, Tang D 2004. Molecular evidence of an interaction between prenatal environmental exposures and birth outcomes in a multiethnic population. Environ Health Perspect. 2004 Apr;112(5):626-30.

Phillips ML 2006. Registering Skepticism: Does the EPA's Pesticide Review Protect Children? Environ Health Perspect. 2006 Oct;114(1):A592-A595.

Rauh VA, Garfinkel R, Perera FP, Andrews HF, Hoepner L, Barr DB, Whitehead R,
Tang D, Whyatt RW 2006. Impact of prenatal chlorpyrifos exposure on neurodevelopment in the first 3 years of life among inner-city children. Pediatrics. 2006 Dec;118(6):e1845-59. Epub 2006 Nov 20.

Rauh VA, Whyatt RM, Garfinkel R, Andrews H, Hoepner L, Reyes A, Diaz D, Camann D, Perera FP 2004. Developmental effects of exposure to environmental tobacco smoke and material hardship among inner-city children. Neurotoxicol Teratol. 2004 May-Jun;26(3):373-85.

Whyatt RM, Barr DB, Camann DE, Kinney PL, Barr JR, Andrews HF, Hoepner LA, Garfinkel R, Hazi Y, Reyes A, Ramirez J, Cosme Y, Perera FP 2003. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns. Environ Health Perspect. 2003 May;111(5):749-56.

Whyatt RM, Camann D, Perera FP, Rauh VA, Tang D, Kinney PL, Garfinkel R, Andrews H, Hoepner L, Barr DB 2005. Biomarkers in assessing residential insecticide exposures during pregnancy and effects on fetal growth. Toxicol Appl Pharmacol. 2005 Aug 7;206(2):246-54.

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