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Additional analysis of these data by Environmental Health Associates (EHA, 1986) and sponsored by
the Shell Oil Company did not show the above association. These data included corrections for
ethnicity. This study used a different method for estimating DBCP concentrations. Although the
associations between cancer incidence and DBCP exposure failed to reach significance at the p < 0.05
level in the EHA study, the magnitude of the associations in the high and low exposure groups were
approximately the same as described in the Jackson et al. (1982) study. The trend for cancer risk and
DBCP exposure is most closely related to the time of residence of the test subjects (Table 1).
Table 1. Relative risk of human gastric cancer in areas with high 1 concentrations of DBCP in the
drinking water compared with areas of low 2 DBCP (Jackson et al., 1982).
Time of Residence
Relative Risk for Gastric Cancer
1 year at death 1.29
1 year prior to death 1.55
10 years prior to death 3.05
1 DBCP concentrations greater than 1.0 ppb.
2 DBCP concentrations less than 0.05 ppb.
Animal Studies
DBCP is a carcinogen in at least two laboratory rodent species by inhalation, ingestion, or dermal
exposure. Tumors following DBCP exposure can arise not only at the site of application, but also at
distal sites. Because of its carcinogenicity to multiple species, DBCP is assumed to represent a
carcinogenic threat to humans (CDHS, 1985).
Three sets of long-term bioassays using mice and rats were conducted respectively by the National
Cancer Institute (NCI, 1978), the National Toxicology Program (NTP, 1982) and Hazelton
Laboratories (1977, 1978). In the NCI (1978) study, DBCP was administered by oral gavage to both
sexes of rats and mice. Two major problems with this study, early mortality and nearly 100%
forestomach carcinoma rate, precluded its usefulness in determining a cancer potency value. The
inhalation study by NTP (1982) had much better survival rates than those observed in the gavage study,
and carcinogenicity was observed for tissues at or near the site of the initial chemical contact.
In the NTP study, groups of 50 B6C3F1 mice or 50 F344 rats of either sex were exposed by inhalation
to 0, 0.6 or 3.0 ppm DBCP for 6 hours/day, 5 days/week, for 76-103 weeks. Surviving high-dose rats
were killed at week 84. High-dose female mice and low- and high-dose male mice were killed at week
76. Low-dose rats and female mice were killed at week 104. A significant increase in the combined
incidence of nasal tumors was found in male and female rats at both concentrations (Table 2a, 2b). In
mice, the combined incidence of nasal tumors was significantly increased in females at both
concentrations, and in males exposed to the high concentration. Proliferative lesions were observed at
sites distal to the lung in the mice, including the kidney, forestomach, and spleen.
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