Urban and Suburban Children’s Exposure to Pyrethroid Pesticides.

Pyrethroids, a group of synthetic insecticides, were manufactured in the 1970s after the removal of organochlorine insecticides, such as DDT, from the consumer market. The synthetic pyrethroids not only inherit the biologic activity (ability to kill insects) from their natural counterpart, pyrethrin, which is found in chrysanthemums, but are also improved in their environmental stability. Pyrethroids are widely used in agriculture, forest, textile industry, and public health programs worldwide. With the phaseout of organo-phosphorus (OP) pesticide use in residential environments in the United States, the availability of pyrethroids for consumer uses has increased since the late 1990s.

Although individual pyrethroid insecticides share some common physical and chemical properties as a group, their toxicologic mechanisms, unlike those of OP pesticides, vary in mammals. Pyrethroid insecticides are subject for review as potential developmental neurotoxicants because of their mode of action on voltage-sensitive sodium channels. In addition, permethrin, the most widely used pyrethroid insecticide, is suspected to be an endocrine-disrupting chemical and, along with fenvalerate, has been classified as a potential carcinogen at high exposure levels. Toxicologic studies have also suggested that pyrethroids have a suppressive effect on the immune system and may cause lymph node and spleen damage.

Although pyrethroids have been sold in the U.S. consumer market for more than 30 years, with the estimated annual use ranging from several thousand to a million pounds, very few studies have been conducted to quantitatively assess human exposures to pyrethroids. Most of the relevant data were obtained from studies conducted in Germany or in occupational settings. Recently, the Centers for Disease Control and Prevention (CDC) reported urinary pyrethroid metabolite levels for the U.S. population 6–59 years of age in the Third National Report on Human Exposure to Environmental Chemicals, which is part of the National Health and Nutrition Examination Survey (NHANES) conducted in 2001–2002. All of these studies were conducted cross-sectionally, so the results represent exposures only over relatively short time periods.

Discussion

Despite the wide use of pyrethroid pesticides, the assessment of pyrethroid pesticide exposure in the U.S. population, particularly for children, is limited to a handful of cross-sectional studies. This report consists of data collected as part of the ongoing CPES with a focus on children’s exposure to pyrethroid pesticides. This longitudinal data set provides a more complete documentation of children’s exposure to pyrethroids and examines potential risk factors for higher exposure levels.

The most significant finding of this study—the association between self-reported pyrethroids use in the residential environment by the parents and the elevated pyrethroid metabolite levels found in their children’s urine—is important for both children’s pesticide exposure assessment and environmental public health. Interventions could focus on minimizing the use of pyrethroids in the residential environment or eliminating the possible contact with treated areas or objects by children. This finding is consistent with those of a previous report suggesting that children whose parents reported residential OP pesticide use had higher OP urinary metabolite concentrations. Although changing children’s diets from conventional to organic food also lowers their exposures to pyrethroid pesticides, the effect of such dietary intervention is not as dramatic for pyrethroid pesticides as it is for OP pesticides. This pattern is in agreement with the general theory that children are exposed continuously to low levels of pesticides through their diets and that this chronic exposure is modified, usually increased, by episodes of relatively high exposures from other pathways, such as residential use.

We conclude that residential pesticide use represents a very important risk factor for children’s exposure to pyrethroid insecticides. This conclusion is supported by the fact that only seven of the 23 families reported residential pyrethroid use, yet such use accounted for more of the variability in the urinary pyrethroid metabolites than did the dietary intervention. The results from the mixed-effects model indicated that residential use of pyrethroids remains a more significant predictor of both urinary PBA and trans-DCCA when different diets were taken into account. The data presented clearly demonstrate that children who lived in households where pyrethroids have been used for pest control purposes have experienced much higher pyrethroid exposures than those whose parents reported no pyrethroid use in their homes. Four of the five highest pyrethroid metabolite levels were found in these seven children.

An extreme case was that of a 4-year-old child whose parents used permethrin on the furniture, including beds. Several urine samples collected from this participant have the highest DVWA PBA and cis- and trans-DCCA levels. Other children who lived in homes where pyrethroids were used were continuously exposed to this group of insecticides throughout the 15-day study period. Notably, our pesticide use survey asked whether pesticides are used in and around the home and, if so, when the last application occurred. Thus the continuous exposure to these pesticides throughout the 15-day study period likely reflects residual sources.

Children were also exposed to pyrethroids through diets, although the magnitude was smaller than the residential exposure. Results from studies conducted in Germany have suggested that exposure to pyrethroids in the general population is caused by uptake with the diet; however, no direct evidence was provided to support this conclusion. In our study, all five of the measured pyrethroid metabolites were found during the organic diet period, including the two least frequently detected metabolites, FPBA and DBCA, specific metabolites for cyfluthrin and deltamethrin, respectively. Accordingly, most of the children’s exposures to pyrethroid metabolites are likely to have come from the environment.

In this study, age is a significant predictor for pyrethroid exposure. We found that older children, 8–11 years of age, experienced higher pyrethroid exposures than did children 3–7 years of age. This finding is not consistent with results from other studies, which suggest that younger children tend to have higher pesticide exposure than older children. Younger children are more vulnerable to adverse health risks resulting from pesticide exposures because of the difference in their physiologic functions relative to older children and adults. However, it is difficult to draw an absolute conclusion that younger children have higher pesticide exposures, particularly exposures from residential environment, than older children. Although common characteristics of young children, such as hand-to-mouth behaviors and close proximity to the floor, put them at higher risk of pesticide exposure, it is the pesticide residues found in the environment that serve as the prerequisite for exposure and the subsequent oral ingestion.

In this study, we identified residential use as the primary source of the children’s pyrethroid exposure; however, this risk factor itself does not explain the age effect because age accounts for more variability in urinary metabolites than does residential use in the expanded mixed-effects model. One plausible explanation for this finding is that, as reported by their parents, many older children in this study were engaged in outside sports activities, such as swimming or playing tennis, in a neighborhood country club and parks during this sampling period.

Pyrethroids used in those facilities may have led to increased pyrethroid exposure. With the regulation change that led to the restricted use of OP pesticides in residential environments, previously we were able to demonstrate that children are exposed to OP pesticides exclusively from their diets. Because fewer regulatory restrictions are imposed on the pyrethroid use, results from this study suggest that this same group of children are simultaneously exposed to pyrethroids via dietary intake and from their residential environments. Such diverse exposure patterns among children may pose a challenge for regulating pyrethroid insecticides as a group under the Food Quality Protection Act of 1996, which mandates the assessment of exposure in an aggregate manner. The implementation of the Food Quality Protection Act (1996) for pyrethroids could be even more problematic because of the difficulties of assessing cumulative risks resulting from pyrethroid exposures. Unlike OP or carbamate pesticides, pyrethroids do not appear to exhibit a single common toxicologic mechanism in humans.

Besides the limitations associated with this study that were discussed previously, the lack of environmental measures for pyrethroids makes it difficult to confirm the association between children’s exposure to pyrethroids and their residential use. Systematic quantification of pyrethroids and other nonpersistent pesticides, such as OP, in the environment, via soil, house dust, surface wipe, or personal breathing air collection, remains a daunting task. Substantial numbers of samples are needed to minimize the spatial and temporal variations, which is commonly associated with the measurements of nonpersistent pesticide exposures. The cost for analyzing such large numbers of environmental samples would compromise other aspects of a study with a limited research budget, such as reducing the number of participants or collecting less frequent biologic samples.

Conclusion

We report the results from the first study of urban/suburban children’s longitudinal exposure to pyrethroid pesticides. In this study we found elevated urinary levels of pyrethroid metabolites associated with both residential pyrethroid use and diets. Pyrethroid use in the residential environment is a particular concern not only because exposures were routinely measured during the days when children consumed an organic diet but also because urine samples collected from this subgroup of children contained the highest levels of four pyrethroid metabolites. These findings provide an opportunity for intervention: The association between self-reported residential use of pyrethroids and the elevated pyrethroid metabolite levels found in the children can be broken by either minimizing the use of pyrethroids in the residential environment or eliminating children’s possible contact with treated areas or objects.