Phthalates

Introduction

Characteristic of the Agent

Fate and Transport

Environmental Impacts

Environmental Monitoring

Exposure Pathway

Routes of Exposure

Methods for Measuring Human Exposure

Strategies for Preventing or Controlling Exposures



Harmful Effects

Dose Response

Absorption, Distribution and Metabolism

Biomarkers

Target Organs and Tissues

Mechanisms of Toxicity

Risk Assessment and Risk Management

References

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RISK ASSESSMENT and RISK MANAGEMENT

RISK ASSESSMENT

  • DEHP and its metabolites can be measured in the blood and urine to confirm recent exposure. In case of monitoring purposes urine samples are preferred as discussed in the biomarker section.
  • Considering the lipophilicity of DEHP and its tendency to migrate into adipose deposits, analysis of concentration of DEHP in fat tissues probably provides the best test for previous exposure to this plasticizer. XIX
  • As written in the Lowell Report XIX, There is a general lack of adequate human toxicity or epidemiologic studies to determine whether DEHP exposure is associated with adverse outcomes in humans, despite the compound’s high volume production, documented human exposure, and documented adverse effects in animals. The lack of epidemiologic studies is at least partly explained by:
    (1) Difficulty in following high risk groups, such as premature infants, because of long latent periods between exposures and possible effects;
    (2) Impacts of DEHP exposure may be subtle (ie: partial loss in sperm production);
    (3) Considerable variability in human exposure levels and the difficulty in measuring human exposure adequately
    (4) The ubiquity of phthalate exposure in the environment, which means that humans are exposed to DEHP through many different routes, making it difficult to distinguish exposed and unexposed groups.

The International Agency for Research on Cancer (IARC) made an assessment for DEHP and stated the following: XXXVI

  • There is inadequate evidence in humans for the carcinogenicity of
    di(2-ethylhexyl) phthalate.
  • There is sufficient evidence in experimental animals for the carcinogenicity of di(2-ethylhexyl) phthalate.

Overall evaluation

  • Di(2-ethylhexyl) phthalate is not classifiable as to its carcinogenicity to humans

This evaluation was based on the understanding that tumors in rodent studies did not involve DNA reactivity, but peroxisome proliferation. This same mechanism did not occur in human liver cultures or in non-human primates. Their conclusion was that peroxisome proliferation was not relevant to humans. Risk assessment for phthalate exposures are complex as described above by both the Lowell Report and the International Agency for Research on Cancer (IARC). More human data collection and animal/human dose-response extrapolation research is needed to help define the risk.

RISK MANAGEMENT

  • Possible elimination or reduction the amount of phthalate esters used in industries; Strategies for Preventing or Controlling Exposures are found earlier in the site
  • If possible use less harmful material in the manufacturing process;
  • In the case of phthalate esters occurring in workplace or environment protective measures should be given including use of protective equipment, regular monitoring for air samples, establishment of maximal exposure level (MEL), regular physical examination of the people exposed to this material to find out the adverse health effects and susceptibility people;
  • In case of poisoning several methods should be adopted to reduce toxic effects. After acute dermal or ocular exposure due to DEHP spills or other accidents, contaminated clothing should be removed and exposed skin thoroughly washed with soap and water. Exposed eyes should be flushed with a clean neutral solution such as water or saline. A number of strategies are involved to minimize absorption from the gastrointestinal tract following acute high dose ingestion and reduce body burden and interfere with the mechanism of action for toxic effects. Gastric lavage can remove DEHP from the stomach if the ingestion was recent (within 60 minutes). Ingestion of activated charcoal is one method for reducing the intestinal absorption of DEHP since DEHP will adsorb to the carbon surface and be excreted with the fecal matter. Another method for reducing absorption is the use of a cathartic; Activated charcoal is frequently given as a slurry in saline or sorbitol cathartics. Specific DEHP-binding or DEHP-reactive agents which might prevent absorption are currently not available. XXI
  • State and Federal regulations stated earlier in this website. Please see Environmental monitoring for these regulations. With the increasing use of plastics in daily life, the amounts of phthalates being used are also ever increasing. Tightening regulations and better enforcement of these laws controlling occupational/public exposures, as well as promoting alternative strategies to reduce exposure levels, can help to minimize the concerns and threats phthalates compounds may pose to humans and nature.

As mentioned in this website, the concerns for the health effects are very much in dispute. The people at the highest risk levels are those using medical equipment. This population, although still under the LOAEL of rodent models, clearly are benefiting from the flexible plastics products. This population is a small population at risk, and many times the risk being of acute exposure. Further research is needed on phthalates with a greater emphasis on chronic human exposures to the compounds. This may yield vast information to help understand the impacts these compounds have in human health. Due to the majority of the information on phthalates using animal models, the extrapolations between the model animal and humans is key to understanding.