Dibromochloropropane (1,2-dibromo-3-chloropropane, DBCP), a
pesticide used widely for over 20 years to control nematodes on crops, turf and in nurseries, was banned by the United States Environmental Protection Agency (US EPA) in 1977 because of evidence of
infertility in men and induction of a variety of
tumors in laboratory animals. Despite the ban on the use of
DBCP, this
pesticide remains persistent in soil and continues to be detected as a groundwater contaminant in areas of past high use, in particular California's Central Valley. In this review, we present a critical evaluation of the available scientific literature on the potential for
DBCP to affect
cancer risk, including the results of animal
cancer bioassays, human epidemiological studies and in vitro and in vivo genotoxicity studies. In addition, we provide updated information on
DBCP chemistry and metabolism, production and past use, current regulations, its environmental fate, potential for human exposure and current remediation efforts. Results from long-term
cancer bioassays in rodents show a statistically significant increase in the incidence of malignant and benign mammary gland
tumors in female rats treated orally with
DBCP compared to controls and some evidence of increased incidence of mammary
fibroadenomas in
DBCP low-dose treated female rats exposed by inhalation. Significantly increased incidence of
tumors of the forestomach occurred in both sexes of rats and mice treated orally. Rats exposed to
DBCP by inhalation showed significant increases in
tumors of the tunica vaginalis in males;
tumors of the pharynx and adrenal gland in females; and
tumors of the tongue, nasal turbinate and nasal cavity in both sexes compared to controls. Male and female mice exposed to
DBCP by inhalation experienced increased
tumor incidence in the lungs and nasal cavity compared to controls. Significant increases in
tumors of the lung and forestomach have also been reported in female mice treated by a dermal route. Although high mortality rates in both rat and mouse bioassays limited the ability to detect
tumors late in life, the induction of a variety of
tumors by multiple routes of exposure in two rodent species provides clear evidence of a
DBCP tumorigenic response. In vitro, in vivo and human genotoxicity studies indicate that
DBCP is capable of acting as a
mutagen and
clastogen. Few studies have been conducted to assess whether
DBCP workplace or
drinking water exposures affect
cancer risk in humans. While case-control, cohort and ecological epidemiology studies have not found significant, positive associations between
DBCP exposure and
cancer in exposed populations, these studies have numerous limitations including small numbers of participants, a lack of control for confounding factors, lack of exposure information on
DBCP and other chemicals and short follow-up times. Given the persistent nature of
DBCP contamination in areas of past use, efforts should be made to continue remediation efforts and follow previously exposed populations for development of certain human
cancers, including breast, ovarian, stomach, respiratory, oral and
nasal cancers, among others.