Human data epidemiological studies

There are no data to verify if the above chronic effects seen in animals are also seen in humans. No epidemiological studies of cancer have been conducted. 

Hecdth effects data come from three types of studies clinical, epidemiological, and toxicological. Clinical and epidemiological studies focus on human subjects, whereas toxicological studies are conducted on animals or simpler cellular systems. Ethical considerations limit human exposure to low levels of air poUutants which do not have irreversible effects. Table 7-1 lists the advantages and disadvantages of each type of experimental informahon. 

The number of clear human epidemiologic studies is small. A total of approximately 50 compounds (c.g., benzene, vinyl chloride) and complex e.xposures (e.g., aluminum production, tobacco smoke) have sufficient data available to permit their classification as human carcinogens. The most potent human carcinogens known, the aflatoxins. are of natural origin. Their presence in food products through infestation by toxin-producing fungi constitute a serious problem in several tropical and subtropical countries. 

Epidemiological and Human Dosimetry Studies. Epidemiological studies of radiation dose typically involve estimates of exposure that are based on whole-body measurements of internally-deposited americium. A need remains for epidemiological data that can provide quantitative human dose-response information while supplying additional information on the health effects of exposure to ionizing radiation and americium in particular, for cases of known internal exposure. 

According to EPA (IRIS 1999), the available human epidemiological studies lack quantitative exposure data for lead and for possible confounding exposures (e.g., arsenic, smoking). Cancer excesses in the lung and stomach of lead-exposed workers that are reported are relatively small, dose-response relationships are not demonstrated neither is there consistency in the site of cancers reported. EPA (IRIS 1999) concluded that the human data are inadequate to refute or demonstrate the potential carcinogenicity of lead exposure. 

No acute-, intermediate-, or chronic-duration inhalation MRLs were derived for cyanide because of the limitations associated with the available studies. Many of the animal and human studies used lethality, or serious effects, such as coma, as the end point. Two epidemiological studies are available however, one study lacked good exposure data, and the other study involved occupational exposure in the electroplating industry where exposure to other chemicals may have occurred. 

We would, of course, prefer not to see anything but negative results from epidemiology studies. In an ideal world information on toxic properties would be collected before human exposure is allowed to take place, and that information would be used to place limits on the amount of human exposure that is permissible. If mechanisms existed to enforce those limits, then excess chemical risk would not occur and, it obviously follows, would not be detectable by the epidemiologist (unless, of course, the data or methods for setting limits were in error). 

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