Alleged misconceptions' distort perceptions of environmental cancer risks.
In a series of papers, Ames and colleagues allege that the scientific and public health communities have perpetuated a series of 'misconceptions' that resulted in inaccurate identification of chemicals that pose potential human cancer risks, and misguided cancer prevention strategies and regulatory policies. They conclude that exposures to industrial and synthetic chemicals represent negligible cancer risks and that animal studies have little or no scientific value for assessing human risks. Their conclusions are based on flawed and untested assumptions. For instance, they claim that synthetic residues on food can be ignored because 99.99% of pesticides humans eat are natural, chemicals in plants are pesticides, and their potential to cause cancer equals that of synthetic pesticides. Similarly, Ames does not offer any convincing scientific evidence to justify discrediting bioassays for identifying human carcinogens. Ironically, their arguments center on a ranking procedure that relies on the same experimental data and extrapolation methods they criticize as being unreliable for evaluating cancer risks. We address their inconsistencies and flaws, and present scientific facts and our perspectives surrounding Ames' nine alleged misconceptions. Our conclusions agree with the International Agency for Research on Cancer, the National Toxicology Program, and other respected scientific organizations: in the absence of human data, animal studies are the most definitive for assessing human cancer risks. Animal data should not be ignored, and precautions should be taken to lessen human exposures. Dismissing animal carcinogenicity findings would lead to human cancer cases as the only means of demonstrating carcinogenicity of environmental agents. This is unacceptable public health policy.
Tomatis
L
L
National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709, USA.
Melnick
R L
RL
Haseman
J
J
Barrett
J C
JC
Huff
J
J
D000818:Animals; D002273:Carcinogens / Q000009:adverse effects / Q000138:chemical synthesis / Q000494:pharmacology / Q000633:toxicity*; D004195:Disease Models, Animal; D004305:Dose-Response Relationship, Drug; D004777:Environment; D004781:Environmental Exposure; D004787:Environmental Pollution / Q000009:adverse effects; D005260:Female; D015386:Hazardous Substances / Q000009:adverse effects / Q000138:chemical synthesis / Q000494:pharmacology / Q000633:toxicity; D006727:Hormone Antagonists / Q000138:chemical synthesis / Q000494:pharmacology / Q000633:toxicity; D006801:Humans; D008297:Male; D023421:Models, Animal; D009369:Neoplasms / Q000139:chemically induced / Q000453:epidemiology / Q000209:etiology; D010575:Pesticides / Q000009:adverse effects / Q000138:chemical synthesis / Q000494:pharmacology / Q000633:toxicity; D011634:Public Health / Q000193:education / Q000379:methods / Q000592:standards*; D011640:Public Policy; D015203:Reproducibility of Results; D018570:Risk Assessment; D014116:Toxicology / Q000379:methods / Q000592:standards* / Q000706:statistics & numerical data
D002273:Carcinogens; D015386:Hazardous Substances; D006727:Hormone Antagonists; D010575:Pesticides