Background Polyvinyl chloride plastics (PVC), made¯exible through the addition of di-2-ethylhexyl phthalate (DEHP), are used in the production of a wide array of medical devices. From the late 1960s, leaching of DEHP from PVC medical devices and ultimate tissue deposition have been documented. Methods A critical review of DEHP exposure, metabolism, and toxicity data from human and animals studies was undertaken. A brief analysis of alternatives to DEHP-plasticized PVC for use in medical device manufacture was completed. Results DEHP leaches in varying concentrations into solutions stored in PVC medical devices. Certain populations, including dialysis patients and hemophiliacs may have long-term exposures to clinically important doses of DEHP, while others, such as neonates and the developing fetus, may have exposures at critical points in development. In vivo and in vitro research links DEHP or its metabolites to a range of adverse effects in the liver, reproductive tract, kidneys, lungs, and heart. Developing animals are particularly susceptible to effects on the reproductive system. Some adverse effects in animal studies occur at levels of exposure experienced by patients in certain clinical settings. DEHP appears to pose a relatively low risk of hepatic cancer in humans. However, given lingering uncertainties about the relevance of the mechanism of action of carcinogenic effects in rodents for humans and interindividual variability, the possibility of DEHPrelated carcinogenic responses in humans cannot be ruled out.Conclusions The observed toxicity of DEHP and availability of alternatives to many DEHP-containing PVC medical devices presents a compelling argument for moving assertively, but carefully, to the substitution of other materials for PVC in medical devices. The substitution of other materials for PVC would have an added worker and community health bene®t of reducing population exposures to DEHP, reducing the creation of dioxin from PVC production and disposal, and reducing risks from vinyl chloride monomer exposure.

Background Polyvinyl chloride plastics (PVC), made flexible through the addition of di‐2‐ethylhexyl phthalate (DEHP), are used in the production of a wide array of medical devices. From the late 1960s, leaching of DEHP from PVC medical devices and ultimate tissue deposition have been documented. Methods A critical review of DEHP exposure, metabolism, and toxicity data from human and animals studies was undertaken. A brief analysis of alternatives to DEHP‐plasticized PVC for use in medical device manufacture was completed. Results DEHP leaches in varying concentrations into solutions stored in PVC medical devices. Certain populations, including dialysis patients and hemophiliacs may have long‐term exposures to clinically important doses of DEHP, while others, such as neonates and the developing fetus, may have exposures at critical points in development. In vivo and in vitro research links DEHP or its metabolites to a range of adverse effects in the liver, reproductive tract, kidneys, lungs, and heart. Developing animals are particularly susceptible to effects on the reproductive system. Some adverse effects in animal studies occur at levels of exposure experienced by patients in certain clinical settings. DEHP appears to pose a relatively low risk of hepatic cancer in humans. However, given lingering uncertainties about the relevance of the mechanism of action of carcinogenic effects in rodents for humans and interindividual variability, the possibility of DEHP‐related carcinogenic responses in humans cannot be ruled out. Conclusions The observed toxicity of DEHP and availability of alternatives to many DEHP‐containing PVC medical devices presents a compelling argument for moving assertively, but carefully, to the substitution of other materials for PVC in medical devices. The substitution of other materials for PVC would have an added worker and community health benefit of reducing population exposures to DEHP, reducing the creation of dioxin from PVC production and disposal, and reducing risks from vinyl chloride monomer exposure. Am. J. Ind. Med. 39:100–111, 2001. © 2001 Wiley‐Liss, Inc.

Human milk is the best source of nutrition for infants. Breast milk contains the optimal balance of fats, carbohydrates, and proteins for developing babies, and it provides a range of benefits for growth, immunity, and development. Unfortunately, breast milk is not pristine. Contamination of human milk is widespread and is the consequence of decades of inadequately controlled pollution of the environment by toxic chemicals. The finding of toxic chemicals in breast milk raises important issues for pediatric practice, for the practice of public health, and for the environmental health research community. It also illuminates gaps in current knowledge including a) insufficient information on the nature and levels of contaminants in breast milk; b) lack of consistent protocols for collecting and analyzing breast milk samples; c) lack of toxicokinetic data; and d) lack of data on health outcomes that may be produced in infants by exposure to chemicals in breast milk. These gaps in information impede risk assessment and make difficult the formulation of evidence-based health guidance. To address these issues, there is a need for a carefully planned and conducted national breast milk monitoring effort in the United States. Additionally, to assess health outcomes of toxic exposures via breast milk, it will be necessary to examine children prospectively over many years in longitudinal epidemiologic studies that use standardized examination protocols that specifically assess breast milk exposures. Finally, current risk assessment methods need to be expanded to include consideration of the potential risks posed to infants and children by exposures to chemical residues in breast milk.

A growing body of research confirms the existence of a powerful connection between socioeconomic status and health. This research has implications for both clinical practice and public policy and deserves to be more widely understood by physicians. Absolute poverty, which implies a lack of resources deemed necessary for survival, is self-evidently associated with poor health, particularly in less developed countries. Over the past two decades, economic decline or stagnation has reduced the incomes of 1.6 billion people. Strong evidence now indicates that relative poverty, which is defined in relation to the average resources available in a society, is also a major determinant of health in industrialized countries. For example, persons in U.S. states with income distributions that are more equitable have longer life expectancies than persons in less egalitarian states. There are numerous possible approaches to improving the health of poor populations. The most essential task is to ensure the satisfaction of basic human needs: shelter, clean air, safe drinking water, and adequate nutrition. Other approaches include reducing barriers to the adoption of healthier modes of living and improving access to appropriate and effective health and social services. Physicians as clinicians, educators, research scientists, and advocates for policy change can contribute to all of these approaches. Physicians and other health professionals should understand poverty and its effects on health and should endeavor to influence policymakers nationally and internationally to reduce the burden of ill health that is a consequence of poverty.