Regarding the negative effects of plastics on the human population, there is a growing literature on potential health risks. A variety of chemicals used in the production of plastics are known to be toxic. Biomonitoring (for example, measuring the concentration of environmental pollutants in human tissue) provides an integrated measure of an organism’s exposure to pollutants from multiple sources.
This approach has shown that chemicals used in the production of plastics are present in the human population and studies using laboratory animals as model organisms indicate potential negative health effects of these chemicals (Talsness et al. 2009). The body burden of chemicals used in plastic manufacturing has also been related to adverse effects on the human population, including reproductive abnormalities (e.g., Swan et al. 2005; Swan 2008; Lang et al. 2008).
Interpreting biomonitoring data is complex and a key task is to put the information into perspective with dose levels that are considered toxic based on experimental studies on laboratory animals. The concept of ‘toxicity’, and therefore experimental methods for studying the health impacts of chemicals in plastics and other chemicals classified as endocrine disruptors, is currently undergoing a transformation (a paradigm reversal) as the disruption of Endocrine regulation systems require very different approaches from the study of acute toxins or poisons. Therefore, there is ample evidence that traditional toxicological approaches are inadequate to reveal outcomes such as “reprogramming” of molecular systems in cells following exposure to very low doses during critical developmental periods (e.g., Myers et al. 2009) . Research on experimental animals informs epidemiologists about the potential for adverse effects on humans and thus plays a vital role in chemical risk assessments. A key conclusion of the article by Talsness et al. (2009) is the need to change our approach to chemical testing for risk assessment. As these authors and others have noted, it is necessary to integrate endocrinology concepts into the assumptions underlying the chemical risk assessment. In particular, the assumptions that dose-response curves are monotonous and that threshold doses (safe levels) exist are neither true for endogenous hormones nor for hormonally active chemicals (which include many chemicals used in plastics) ( Talsness et al. 2009). ).
The biomonitoring approach has shown that phthalates and BPA, as well as other additives in plastics and their metabolites, are present in the human population. It also showed that the most common human exposure scenario is that of a large number of these chemicals at the same time. These data indicate differences in geographic location and age, with higher concentrations of some of these chemicals in young children. Although exposure through house dust is extensive (Rudel et al. 2008), it would appear that at least for some phthalates (eg, diethylhexyl phthalate, DEHP), food and, to a lesser extent, drug use Oral probably present important pathways of absorption (Wormuth et al. Al. 2006). Data on BPA exposure are similar but less extensive. While the mean concentrations of phthalates in selected populations around the world seem fairly similar, there is evidence of considerable variability in daily intake rates between individuals and also within individuals (Peck et al. 2009). Ingestion, inhalation and exposure by skin contact are considered important routes of exposure for the general population (Adibi et al. 2003; Rudel et al. 2003). Koch and Calafat (2009) show that while mean / median exposure for the general population was below the levels determined to be safe for daily exposure (US, EPA reference dose, RfD; and EU tolerable daily intake ), the higher percentiles of Di-butylphthalate and urinary metabolite DEHP concentrations show that for some people the daily intake may be substantially higher than previously assumed and may exceed the estimated safe daily exposure levels.