Pesticides and children

Abstract

Prevention and control of damage to health, crops, and property by insects, fungi, and noxious weeds are the major goals of pesticide applications. As with use of any biologically active agent, pesticides have unwanted side-effects. In this review, we will examine the thesis that adverse pesticide effects are more likely to occur in children who are at special developmental and behavioral risk. Children's exposures to pesticides in the rural and urban settings and differences in their exposure patterns are discussed. The relative frequency of pesticide poisoning in children is examined. In this connection, most reported acute pesticide poisonings occur in children younger than age 5. The possible epidemiological relationships between parental pesticide use or exposure and the risk of adverse reproductive outcomes and childhood cancer are discussed. The level of consensus among these studies is examined. Current concerns regarding neurobehavioral toxicity and endocrine disruption in juxtaposition to the relative paucity of toxicant mechanism-based studies of children are explored.

Introduction

For many years now, there has been public concern raised about the potential health effects of pesticides on the developing fetus and in childhood. Depending on stage of development, the fetus is selectively sensitive to particular chemical toxicants Schardein, 1993, Wilson and Fraser, 1977.

In the postnatal period and through pubescence, children are vulnerable to their environment, whether physical, chemical, or psychological. Less clear is the relative vulnerability of pregnancy due to pre-pregnancy germ cell exposure of adult females and males.

In a recent USEPA summary report (USEPA: EPA/630/R-03/002, 2002, p. F-36), Locke (2002) defined vulnerability applied to risk assessment as a four-component system: (1) susceptibility or sensitivity of the human or ecological receptors; (2) differential exposures of the receptors; (3) differential preparedness of the receptor to withstand the insult from exposure; (4) differential ability to recover from these effects. All of these components are pertinent to systems undergoing development from the fetus through childhood.

For example, differences in the chemical biotransformation capacity of the human fetus and developing child (Hakkola et al., 1998) can be both protective and potentially detrimental to normal development (USEPA/630/r-01/004, 2001). Regarding this point, there is little direct information regarding the specific metabolism of xenobiotics, much less pesticides, in children or the fetus. Overriding differences in biotransformation in the fetus is the probable role of maternal metabolism of xenobiotics affecting the level of fetal toxicant exposure. Polymorphisms of maternal phase 1 and phase 2 enzymes may play a key role in these exposure events (USEPA/630/r-01/004, 2001).

A fundamental maxim of pediatric medicine is that “children are not little adults”. This observation is especially relevant to discussion of children and their exposures to pesticides. Children are at risk for pesticide exposures from different sources and at levels different than adults in the same exposure scenario. Children's respiratory rate, heart rate, and metabolism are significantly different from adults (Bearer, 1995). Food consumption and food consumption patterns place children in a special dietary pesticide risk category (National Academy of Sciences, 1993). Hand-to-mouth behavior further adds to children's pesticide exposure by the oral route. Children, being low to the ground, may have greater exposure to volatile pesticide vapors, particularly those pesticides that, in the gas phase, have a density greater than air. One prime example is the grain fumigant aluminum phosphide (AlP). After enclosed space application, AlP is converted to the toxicant gas phosphine, the active pest control agent. Human phosphine fatality case reports dealing with children playing on AlP fumigated grain, and another dealing with a fatality of a pregnant woman living near large tarp covered fumigated grain piles, illustrate the potential hazard (Garry and Lyubimov, 2001).

In the US, beginning with the conclusions derived from the 1993 National Academy of Science report on pesticides in the diets of infants and children and culminating in 1996 with revision of the US Federal Fungicide, Insecticide and Rodenticide Act (FIFRA) to include the directive “In the case of threshold effects, an additional 10-fold margin of safety for the pesticide chemical residue and other sources of exposure shall be applied for infants and children to take into account potential prenatal and postnatal toxicity (Makris and Rowe, 1998)”, the vulnerability of children to the toxicant effects of pesticides was recognized.

In the review to follow, we will first discuss children's pesticide exposures in the rural and urban environment. Later, we will consider children's cancer and birth defects in relation to pesticide exposure of both parent and child. The plausibility of pesticide-related postnatal neurologic and neurobehavioral effects will be considered. The possible role of endocrine disruption will be summarized.