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therefore, should emphasize safe management in their production and use,
with particular regard to the health of nontarget species and the environment.
The decisions to manufacture and use pesticides are economic and sociopolitical
in nature and require input from two developing sciences: toxicology
and epidemiology. In addition, adequate solutions to the complex problem of
preventing harmful exposure require critical contributions from the social and
behavioural sciences.
Toxicology and epidemiology as
complementary sciences
In the context of occupational and environmental risk assessment, toxicology
and epidemiology address two rather different questions: could it? and did it?
Toxicology is based primarily on animal and cell studies, normally before
human exposure has taken place, whereas epidemiological studies necessarily
follow human exposure. A more complete series of questions relevant to
health-risk analysis would also include: what price? (economics) and should
it? (sociopolitics).
The complementary nature of these scientific disciplines can be appreciated
historically. Epidemiology first revealed such relations as renal cancer to
coke-oven emissions, mesothelioma to asbestos exposure, and phocomelia to
thalidomide (Taussig 1962; Redmond et al. 1972; McDonald 1990). Toxicology
has taken the lead in establishing the risk potential of a wide range of
chemicals and their byproducts, including formaldehyde and nasal septal
cancer in rats, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and renal agenesis
in rabbits, and benzolalpyrene and mutagenesis in cell culture (Giavini et al.
1982; Clary et al. 1983; O'Donovan 1990). Working along parallel paths, the
two disciplines have elucidated particular relations such as in the classic case
of vinyl chloride, shown by toxicology to be carcinogenic in the mouse (liver
and lung), rat (brain), and hamster (lymphatic tissue), whereas virtually
simultaneous epidemiologic studies revealed human cancers at all these sites
(Lilis 1986). However, both disciplines have underlying assumptions,
strengths, and limitations that are important to acknowledge.
Two basic assumptions lie at the foundation of toxicology: that the effects
produced by a chemical in laboratory animals when properly qualified are
applicable to humans, and that it is possible to estimate risks associated with
low-level exposure by observing effects at high-level exposure. The first
assumption is confounded by considerations such as selective toxicity, differing
portals of entry, variations in metabolism and toxicokinetics, questions of
methodology relating to interspecies extrapolation, and complex problems of
multiple exposures in the human setting. Contentious also are the results of
studies in cell cultures, in the absence of host-defence or DNA-repair mechanisms,
and it is difficult to know how to interpret this type of information,
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