| 英文摘要: | Burns et al. (2015) question whether residential proximity to agricultural pesticide applications can serve as a surrogate for actual exposures in research on autism spectrum disorders (ASDs) and neurodevelopmental delay. Previous work has consistently demonstrated that pesticide drift results in elevated levels of these compounds in both indoor air and house dust in residences located near agricultural applications (Fenske et al. 2002; Gunier et al. 2011; Harnly et al. 2005; Ward et al. 2006; Wofford et al. 2014). For example, Wofford et al. (2014) intensively monitored ambient air concentrations for 40 active ingredients or degradation products of pesticides in a California Central Valley city. Air concentrations of the organophosphates chlorpyrifos, diazinon, phosmet, and malathion increased after recent applications within 8 km of the city boundary. Notably, these associations were found despite mitigating factors such as those named by Burns et al. (2015), for example, weather conditions, wind direction, type of formulation, and application method. The temporal correspondence between applications and measured concentrations in air was particularly strong for chlorpyrifos (Wofford et al. 2014), which we found to be associated with an elevated prevalence of ASDs among children exposed in utero (Shelton et al. 2014).
Burns et al. (2015) also assert that levels reaching homes are inadequate to induce adverse effects on the fetus. In fact, between 1996 and 2008 pesticide drift or off-target spraying was associated with 2,945 cases of acute pesticide illness in 11 U.S. states, of which 14% were children under 15 years of age (Lee et al. 2011). Furthermore, one-third of acute pesticide illnesses occurring in U.S. schools in 1998–2002 were attributed to drift exposure from farmland (Alarcon et al. 2005). Thus, considerable evidence shows biologically harmful exposures can and do occur in areas surrounding agricultural fields where pesticides are applied.
With chlorpyrifos detectable in 70.5% of pregnant mothers living in an agricultural area in California (Huen et al. 2012), fetal exposure is surely widespread. Because the fetus cannot metabolize organophosphate chemicals as well as its adult mother can (Chen et al. 2003; Furlong et al. 2006), there is a compelling biological basis for more severe effects once the compound passes through the placenta. Given greater fetal and neonatal vulnerability, these aforementioned results raise quite reasonable concerns for parents and warrant research utilizing proximity to pesticides as an exposure indicator when biological samples are unavailable (Harnly et al. 2005).
Finally, Burns et al. (2015) include several misrepresentations of the scientific literature. For example, a review of behavioral impacts of chlorpyrifos exposure in rodent studies (Williams and DeSesso 2014) is cited to support the argument that doses reaching pregnant women neighboring agricultural fields are too low to cause harm to the human fetus. It is unclear how Burns et al. (2015) extrapolated to draw this conclusion or what assumptions they made regarding comparability of rodent versus human dosing.
Burns et al. (2015) also reference work by Ward et al. (2006), who used a spatial model to predict household carpet dust levels of agricultural pesticides. Ward et al. (2006) reported, “Increasing acreage of corn and soybean fields within 750 m of homes was associated with significantly elevated odds of detecting agricultural herbicides [in house dust] compared with homes with no crops within 750 m.” Yet Burns et al. (2015) state to the contrary, “Proximity to agricultural pesticide application has not been found to translate to corresponding levels of the pesticide in household dust (Curwin et al. 2005; Fenske et al. 2002; Ward et al. 2006).” Other results from these cited articles also are misrepresented: Fenske et al. (2002) reported higher chlorpyrifos in house dust for homes in closer proximity (p = 0.01), and Curwin et al. (2005) detected higher levels in farm homes than in nonfarm homes. |