Environmental Factors Develop Different Patterns of Immune Disease

A 379 should include UV exposure, even absent specific FDA requirements. Our resin data (resins P1. P2, P3, P4, P19, and P18) cited by Kelce and Borgert came from at least three replications of stress­ ing, extraction, and EA assays. As described in our " Methods " and " Supplemental Material, " the assay variance was very small: SEs were typically smaller than the diameter of the data points of the graphed means. The whole series of 49 assays was repeated only once, but no extract exhibited EA; more recent extracts of the same plastics confirm our original results. Kelce and Borgert noted that colorants are " embedded " in plastics. However, " bound " colorants in plastic compounds can and do readily leach from plastics. They are additives, which—like most additives—are only rarely chemically bound to polymers. Hence, con­ cerns about all additives are warranted because any can leach from a plastic product. Regarding broader issues, the objective of our paper was to quantify the prevalence of xeno estrogen release from commonly used plastic products. These data are significant in part to help assess the risk of such products to human health and environmental con­ tamination. Kelce and Borgert cite Charles et al. (2007), who examined some inter­ actions between a small set of phyto estrogens and xeno estrogens. The limited negative results of that study have been contradicted by dozens of other studies (e.g., Patisaul and Jefferson 2010). However, our objective was not to establish definitive links between pub­ lic health issues, environmental pollution, and exposure to xenoestrogens. This relation­ ship is an active research area, and it will take many years to obtain definitive answers. Kelce and Borgert's concerns about the paucity of epidemiological data correlating EA exposure via use of plastics with adverse human health effects is analogous to the long­ standing controversy for tobacco, which is now highly regulated, largely because increas­ ing numbers of epidemiological studies correlated smoking with heart disease and lung cancer. For decades, it was common to hear tobacco industry spokes persons argue that " [epidemiological] correlation does not mean causation " and demand that molecu­ lar, cellular, and/or systemic mechanisms be extensively demon strated before any action, regulatory or otherwise, be taken. One rarely hears spokespersons for the chemical and plastics industry make this argument for release of chemicals having EA from plastics, because the mechanisms by which tobacco has …