User:Iscucchi/Phthalate

Alternatives
Being inexpensive, nontoxic (in an acute sense), colorless, noncorrosive, biodegradable, and with easily tuned physical properties, phthalate esters are nearly ideal plasticizers. Among the numerous alternative plasticizers are Dioctyl terephthalate (DEHT) (a terephthalate isomeric with DEHP) and 1,2-Cyclohexane dicarboxylic acid diisononyl ester (a hydrogenated version of DINP).

Many bio-based plasticizers based on vegetable oil have been developed. They can be substituted for dioctyl phthalate.

An additional colorless alternative to phthalates, Di(isononyl) cyclohexane-1,2-dicarboxylate (DINCH), has been used in high volume for a variety of products used in contact with humans as an alternative plasticizer for DEHP and DINP. Some of these products include medical devices, toys, and food packaging. The phthalate ester alternative, DINCH, is a more hydrophobic substance among other alternatives like bis(2-ethylhexyl) adipate (DEHA) and diisodecyl adipate (DIDA). Since alternative plasticizers are more likely to bind to organic matter and airborne particles indoors, exposure to DINCH primarily occurs through contact with dust and food consumption.

Prevalence and human exposure
Due to the ubiquity of plasticized plastics, the majority of people are exposed to some level of phthalates. For example, most Americans tested by the Centers for Disease Control and Prevention have metabolites of multiple phthalates in their urine. In studies of rodents exposed to certain phthalates, high doses have been shown to change hormone levels and cause birth defects.

Disparities among Minority Populations

The question of how these plastics are affecting the population has arisen as plasticizer use in everyday items has increased. Additionally, if there are any disparities in how these plasticizers may affect minority populations and if they are more susceptible to complications. It has been found that exposure to phthalates is more likely in women and people of color. In one study, researchers looked into potential differences between gender and race as well as potential consequences of this higher phthalate exposure. The study paid particular attention to the relationship between urinary phthalate metabolites and risk factors for diabetes in individuals with no previous diabetes diagnosis.It was found that while there were no statistically significant differences between men and women overall, there were differences between Mexican-Americans, blacks, and whites in terms of the overall risk of disturbance of glucose homeostasis. With Mexican-Americans having a fasting blood glucose (FBG) increase of 5.82 mg/dL, blacks having a fasting blood glucose increase of 3.63 mg/dL, and whites having a fasting blood glucose increase of 1.79 mg/dL, there was evidence of an increased risk for minorities. Overall, the study concludes that phthalates may alter glucose homeostasis and insulin sensitivity, and that different populations may be more severely impacted. Higher levels of some phthalate metabolites were associated with elevated FBG, fasting insulin, and insulin resistance.

In a different study looking at the presence of phthalate metabolites in pregnant women, it was found that non-Hispanic black women and Hispanic women had higher levels of some phthalate metabolites, indicating potential racial disparities in pregnancy outcomes.

Other effects
There may be a link between the obesity epidemic and endocrine disruption and metabolic interference. Studies conducted on mice exposed to phthalates in utero did not result in metabolic disorder in adults. However, "in a national cross-section of U.S. men, concentrations of several prevalent phthalate metabolites showed statistically significant correlations with abnormal obesity and insulin resistance." Mono-ethylhexyl-phthalate (MEHP), a metabolite of DEHP, has been found to interact with all three peroxisome proliferator-activated receptors (PPARs). PPARs are members of the nuclear receptor superfamily. The author of the study stated "The roles of PPARs in lipid and carbohydrate metabolism raise the question of their activation by a sub-class of pollutants, tentatively named metabolic disrupters." Phthalates belong to this class of metabolic disruptors. It is a possibility that, over many years of exposure to these metabolic disruptors, they are able to deregulate complex metabolic pathways in a subtle manner.

In order to build up adipose tissue and establish metabolic homeostasis, it has been established that early childhood and puberty are crucial developmental stages. Exposure to endocrine disruptors, such as phthalates, during these crucial developmental stages may negatively affect adipose tissue function and metabolic homeostasis, increasing the risk of obesity. The prevalence of obesity, particularly in children, is rising, according to mounting evidence, which suggests that increased exposure to phthalates through food packaging materials is to blame. In a study conducted on schoolchildren in China, the concentration of mono-n-butyl phthalate (MnBP) was assessed in urine samples. Additionally, increased exposure to phthalates has been linked to an increase in MnBP. MnBP has been linked to significant increases in weight and obesity in schoolchildren. Significant increases in MnBP concentration were found in the study's urine samples. The disruption of the arginine and proline metabolism associated with this elevated MnBP concentration as a result of phthalate exposure is thought to be a factor in the pathophysiological changes associated with childhood obesity.

Large amounts of specific phthalates fed to rodents have been shown to damage their liver and testes, and initial rodent studies also indicated hepatocarcinogenicity. Following this result, di(2-ethylhexyl) phthalate was listed as a possible carcinogen by IARC, EC, and WHO. Later studies on primates showed that the mechanism is specific to rodents; humans are resistant to the effect. The carcinogen classification was subsequently withdrawn.