Bronchogenic carcinoma in cigarette smokers
Chronic bronchitis, emphysema, and heavy wrinkles in cigarette smokers
Drug-related lupus syndrome in patients taking procainamide
Dangerously lowered blood pressure in patients taking debrisoquine or sparteine
Lung cancer in people exposed to radon
Lung cancer in uranium mine workers
Chloracne, porphyria cutanea tarda in workers exposed to dioxin and other halogenated hydrocarbons
Ataxia, lowered mentality in persons exposed to high levels of lead
Increased risk of chronic myelogenous leukemia in workers exposed to benzene, and of urinary bladder cancer in chemical dye workers
Asthma in children and adults exposed to indoor or outdoor air pollution
Toxicity or malignancy in persons living near a hazardous-waste site
The first six examples in Table 7.1 represent large doses of an environmental agent that can be quite easily documented by a good medical history [e.g., pack-years of smoking (number of cigarette packs smoked per year multiplied by number of years that the person has smoked), quantity of alcohol consumed, length of time and the dose of drug taken, length of time living in a radonexposed house]. The next three examples represent exposures to sun and the outdoors and to chemicals in the workplace; quantitation in these cases is generally more difficult than the first six examples (e.g., "What is the actual number of days worked? Was the exposure identical for all these days? Are we dealing with a single chemical or a mixture of multiple chemicals?"). The last four examples in Table 7.1 depict even fuzzier cases in which a cause-effect correlation can be inferred only by an epidemiological study of large human populations, but such a correlation in a particular individual is often difficult to prove—medically, or in a court of law (e.g., ataxia might occur in one patient whose blood Pb level is more than 3 times lower than that of another who is asymptomatic. "Is the malignancy diagnosed in a worker caused by his/her occupational exposure, or was he/she going to develop it, anyway?" "Is this particular bout of asthma caused by urban pollution, or is it caused by house dust or cockroach dander in the home?").
Not listed in Table 7.1 are the even more ambiguous situations. For example, how often can an environmental disease be caused by minuscule and intermittent exposures—over decades or a lifetime—to "everyday" chemicals (e.g., eating fruit that had been treated with a fungicide, playing on a golf course that had been sprayed with insecticides or herbicides, ingesting canned food having "detectable" amounts of an endocrine disruptor). Toxicity or cancer occurring in individuals with these kinds of exposure are the most problematic for scientists to quantitate and interpret.
In addition to the exposure component, why is it increasingly difficult for a scientist or clinician to be certain of the cause of environmental disease, as one moves down the list in Table 7.1? The answer to this question resides in our genes. It is now clear that, just as we each have a distinctive set of fingerprints, each of us has a novel combination of genes that enable us to be resistant or sensitive to various types of chemical and physical insults. This leads to our own unique underlying genetic predisposition to toxicity or cancer. This field of study was termed ecogenetics by Brewer in the mid-1970s, and a subset of this field (interaction between genes and response to drugs) had been named pharmacogenetics in 1959 by Vogel (1-4). Before examining "gene-environment interactions" in more detail, we will review briefly the essentials of genetics and the fundamentals of exposure and risk estimation.
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