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was associated with chlorine dose (- < 0.05). The risk of colon cancer, calculated as odds ratios, was
over twice as great when the water source was affected by rural runoff. This variable was tested
because of the assumption that rural runoff increased the organic precursors to THMs. While the
association of colon cancer with chlorination and rural runoff factors is provocative, the findings of this
study must be considered inconclusive due to the possible underestimation of risk associated with
misclassification error and spurious contribution from unknown colon cancer risk factors (Young et al.,
1981).
Wilkins and Comstock (1981) conducted a nonconcurrent prospective study to investigate possible
relationships between products of water chlorination and human cancer. Site and sex-specific incidence
rates for malignant neoplasm of liver, biliary passages, kidney, and bladder were constructed from
hospital records, a cancer registry, and death certificates. Incidence rates for cancer of the bladder
among men and cancer of the liver among women were not significant relative to the other exposure
groups among persons using water from the chlorinated surface supply. While the results were only
weakly suggestive, Wilkins and Comstock noted that bladder cancer has been suggestively linked with
chloroform and other indices of THM in drinking water in other studies.
Gottlieb and Carr (1982) studied the potential relationship between chlorination of drinking water and
cancer in 20 south Louisiana parishes. Chlorinated surface water was associated with a significant risk
for rectal cancer (p = 0.012). The odds ratio for rectal cancer in groups receiving high chlorination level
(> 1.09 ppm chlorine) to groups with no chlorinations is 1.53 (95% CI=1.15-2.04) in surface water
supplied areas. Gottlieb and Carr concluded that there appears to be some cancer risk associated with
water chlorination, but definitive studies are needed with respect to the role of industrial confounders
and the importance of co-contaminants.
Lawrence et al. (1984) used a case-control approach to study the association of chloroform exposure
via drinking water to colorectal cancer in white female teachers in upstate New York. Analysis was
based on 395 cases of colon and rectal cancer and 395 control noncancer deaths matched with respect
to age and year of death. No effect of cumulative chloroform exposure on incidence of colorectal
cancer deaths was observed.
Cantor et al. (1987) examined the association between use of chlorinated drinking water and bladder
cancer by a case-control study design. The investigators interviewed 2,982 cases and 5,782 controls in
10 geographic areas of the U.S. Risk of bladder cancer was primarily associated with use of tap water
rather than nontap beverages. Among white males, the coefficients for tap and nontap beverages were
0.176 (p < 0.001) and 0.037 (p = 0.42), and among white females, the coefficients were 0.123 (p =
0.09) and 0.089 (p = 0.39), respectively. It was suggested that nonvolatile components of tap water
may be associated with risk of bladder cancer since both heated and nonheated tap water beverages
were significantly associated with bladder cancer risk among males. The relative risk increased with
increasing tap water intake. While this investigation was quite thorough in many respects, there is a
need for confirmation of these findings. The contribution of chloroform in the etiology of human bladder
cancer in men may be overshadowed by other nonvolatile chemicals present in the drinking water.
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