text: Conclusions
  Only after careful consideration of the biological underpinnings of a truly beneficial response can an exposure be considered for the general population, such as the addition of folic acid to cereals. If a toxic or hazardous pollutant were found to have truly beneficial effects at low dose, then that agent should be tested clinically, go through the U.S. Food and Drug Administration (FDA) approval process, and be regulated as a pharmaceutical for those who might benefit from its use. Certainly, the general population should not be exposed to chemotherapeutic agents that benefit cancer patients. For pharmaceuticals, it is understood that there are trade offs between benefits and risks. For example, although aspirin is a generally well-tolerated pain reliever and is increasingly advocated as a preventative tool for heart attacks and colorectal cancer (Vainio and Miller 2003; Werner et al. 2004), it is also linked to increased risk of gastrointestinal bleeding, cerebral hemorrhage (Werner et al. 2004), and asthma attacks (Jenkins et al. 2004). In addition, aspirin is not recommended for children or teenagers who have or are recovering from chicken pox or flulike symptoms because it can cause debilitating and sometimes lethal Reyes syndrome (U.S. FDA 2003). Individual risks to pharmaceutical agents can be controlled with proper usage; however, increased exposure to environmental toxins presents additional involuntary risks for the general population. Under the latter condition, exposure is inadequately controlled, and there is no mechanism to correct for individual circumstances (e.g., medical condition or age) that may result in harm.
  Although hormetic effects may occur in some instances, it is indeed rare that exposures to toxic, mutagenic, teratogenic, and carcinogenic chemicals, even at low exposure levels, would be risk free and provide health benefits for the general public. Portraying chemicals with numerous adverse effects as having benefits while ignoring their hazards is irresponsible and does not provide full and objective disclosure. In the 1950s doctors prescribed DES to pregnant women to prevent miscarriage and premature births and to produce "bigger and stronger babies" even though DES had been shown to cause damage to reproductive tissues in animals (Dinusson et al. 1948; Dunn and Green 1963; Takasugi and Bern 1964). Human use of DES was banned in the United States in 1971 after the discovery of high rates of rare, clear-cell adenocarcinomas of the vagina and cervix in DES-exposed daughters (Herbst 1981), and later studies showed elevated breast cancer risk in women who took DES during pregnancy (Titus-Ernstoff et al. 2001). Certainly, health policy decisions should be based on scientific evidence and not on speculation of health benefits in order for the general population to avoid repeating the mistakes of the past similar to that of the DES tragedy.
  The claims and projections of health benefits from exposures to environmental toxicants and carcinogens are based on untested assumptions and disregard numerous well-established scientific principles that underpin a public health-protective approach to regulating exposure to toxic substances. If hormesis were used in the decision-making process to allow higher exposures to toxic and carcinogenic agents, this would substantially increase health risks for many, if not most, segments of the general population.
  
entities.text: ['cancer']
entities.type: Pathological_formation
entities.entity_id: PMC-1281265-sec-06_T1
entities.text: ['heart']
entities.type: Organ
entities.entity_id: PMC-1281265-sec-06_T2
entities.text: ['colorectal cancer']
entities.type: Pathological_formation
entities.entity_id: PMC-1281265-sec-06_T3
entities.text: ['gastrointestinal']
entities.type: Organism_subdivision
entities.entity_id: PMC-1281265-sec-06_T4
entities.text: ['cerebral']
entities.type: Organ
entities.entity_id: PMC-1281265-sec-06_T5
entities.text: ['tissues']
entities.type: Tissue
entities.entity_id: PMC-1281265-sec-06_T6
entities.text: ['adenocarcinomas']
entities.type: Pathological_formation
entities.entity_id: PMC-1281265-sec-06_T8
entities.text: ['vagina']
entities.type: Multi-tissue_structure
entities.entity_id: PMC-1281265-sec-06_T9
entities.text: ['cervix']
entities.type: Multi-tissue_structure
entities.entity_id: PMC-1281265-sec-06_T10
entities.text: ['breast cancer']
entities.type: Pathological_formation
entities.entity_id: PMC-1281265-sec-06_T11