Cancer Risk Among Residents of Rhineland-Palatinate Winegrowing Communities - Recent Advances and Issues in Environmental Science - page 104

evaluate the cancer incidence in atrazine-exposed pesticide applicators among 53,943
participants in the Agricultural Health Study. In their study, assessing atrazine expo-
sure by lifetime days of exposure, the RR for bladder cancer is non-significantly ele-
vated to 3.06 (95% CI 0.86-10.81). Assessing atrazine exposure by intensity-weighted
lifetime days, the RR for bladder cancer decreases to 0.85 (95% CI 0.24-2.94). Viel
and Challier [17] analyze the mortality from bladder cancer among French farmers.
While the mortality among farmers is non-significantly lowered (standardized mortal-
ity ratio = 0.96; 95% CI 0.85-1.08), there is a significant association with exposure
to pesticides in vineyards (risk ratio = 1.14; 95% CI 1.07-1.22). According to the
authors, these results could explain the French south-north gradient in bladder cancer,
as vineyards are mainly located in Southern France.
Prostate Cancer
Our finding of an increased prostate cancer risk in potentially pesticide-exposed resi-
dents of winegrowing communities is in accordance with the literature. In a recently
conducted meta-analysis, van Maele-Fabry et al. [15] include 18 epidemiological
studies published between 1984 and 2004. The combined RR for all studies is 1.28
(95% CI 1.05-1.58). According to the authors, no specific pesticide or chemical class
is responsible for the increased risk; nevertheless, the strongest evidence consists for
phenoxy herbicides possibly in relation with dioxin and furan contamination. Van
Maele-Fabry [15] point to the lack of fundamental understanding of the basic biol-
ogy of human prostate cancer: hormones (both androgens and estrogens) would likely
play a role in the etiology or promotion of prostate cancer. Therefore, the authors re-
gard it as plausible that chemicals able to modulate steroid sex hormones as agonists,
antagonists or as mixed agonist-antagonist might contribute to the development of
prostate cancer through hormone-mediated effects. Several pesticides might interfere
with sexual hormones through direct action on receptors but also through indirect non-
receptorial mechanisms.
Limitations
We applied an ecologic study design which does not allow a differentiation between
residential, occupational, and life-style risk factors for cancer. The chief limitation of
ecologic studies is the inability to link exposure with disease in particular individu-
als. A second major limitation of ecologic studies is the lack of ability to control for
the effects of potential confounding factors. Thus, observed risk differences between
communities with different area under cultivation may be due not to varying levels of
pesticide usage, but rather to the independent effect of other confounding variables on
cancer risk. Moreover, our “exposure” categories (small, medium, or large area under
cultivation) represent very crude indicators of the individual exposure; the actual in-
dividual exposure depends on occupation, place of residence at the time of pesticide
spraying, wind direction, and so forth. Furthermore, several tests were performed, in-
troducing a multiple comparison problem (altogether, 270 risk ratios were calculated).
In general, our study design should therefore be regarded as exploratory rather than
hypothesis testing. Due to small numbers, particularly for cancer cases in communities