Acute-Duration Exposure. There are data indicating mild upper respiratory irritation in humans from acute inhalation of borate dusts (Wegman et al. 1991). Information on the effects of a single oral exposure to boron compounds in humans and animals have provided data on lethal effects, while injury to the lungs, brain, kidneys, and liver have been reported in infants (NTP 1987; Smyth et al. 1969; Weir and Fisher 1972; Wong et al. 1964). Many of the human data are derived from case reports involving toxic effects in infants. No adverse health effects have been demonstrated in humans after dermal exposure. However, dermal/ocular effects have been associated with dermal exposure in animals (Wilding et al. 1959). The irritation effects observed were probably due to the exothermic rehydration reaction of the anhydride boron oxide. While existing data are sufficient to identify target organs, additional oral and dermal studies may clarify dose-response relationships in target tissues and identify a threshold for systemic effects due to a single-dose exposure. Human and animal data were not sufficient to derive acute oral and inhalation MRLs. Existing data provide qualitative evidence of toxic effects; however, data gaps exist relative to concentration and effects in the target tissues.
Intermediate-Duration Exposure. No studies were located in humans after intermediate exposure to boron compounds by any route of exposure. Borates are not absorbed through intact skin (Draize and Kelley 1959). No studies were available on dermal or inhalation exposure in animals; however, lethal effects and injury to the gonads, particularly the testes, have been demonstrated after oral exposure (Dixon et al. 1979; Lee et al. 1978; NIEHS 1990b; NTP 1987; Seal and Weeth 1980; Weir and Fisher 1972). Data suggest differences in sensitivity to boron compounds among animal species, with dogs more sensitive than rats or mice (Weir and Fisher 1972). Developmental effects were reported in mice and rats after oral exposure (Heindel et al. 1991). Data are sufficient to develop an intermediate oral MRL. The MRL was based on developmental toxicity in rats (Heindel et al. 1991). Although the MRL value is lower than the average daily intake of boron, it should be noted that recommended daily allowance levels have not been established for boron. Further studies by other routes of exposure would be useful in confirming target tissues (e.g., testes) and effects on the fetus identified by the primary exposure route. Also, these data may be used to further assess the level of confidence in current NOAEL and LOAEL values. Additional data may also provide some insight into the basis for differential susceptibility among species which may be useful in assessing potential human risk.
Chronic-Duration Exposure and Cancer. Limited epidemiologic studies conducted in humans demonstrated that borate dust can affect the upper respiratory tract and cause eye irritation following inhalation (Gabarant et al. 1984, 1985). Data were not sufficient to derive a chronic-duration MRL. No studies were found on oral and dermal exposures in humans. Oral studies in animals demonstrated injury to the gonads and to the developing fetus (NIEHS 1990a; NTP 1987; Weir and Fisher 1972). Existing oral studies are sufficient to rule out effects on other organ systems or tissues (NTP 1987; Weir and Fisher 1972). No studies were found on chronic dermal and inhalation data in animals. Additional studies are needed to identify critical effect levels. Although data are sufficient to develop a chronic oral MRL, a value was not derived. Because developmental toxicity occurred at dose levels less than those for reproductive effects, the intermediate MRL, which is based on developmental toxicity, should be protective against reproductive toxicity following chronic exposure. Additional studies should be useful in assessing the level of confidence in existing NOAEL and LOAEL values.
No epidemiologic studies have been conducted in humans regarding boron exposure and cancer. Well-designed and well-conducted case control or cohort studies would be useful in assessing risk to exposed humans. A long-term oral bioassay in mice was negative. No studies on chronic dermal or inhalation exposure evaluating carcinogenic potential in animals are available. The absence of effects in one species is not sufficient to rule out the potential to cause cancer. Additional chronic studies of other species and various doses would increase the level of confidence in results reported in existing studies.
Genotoxicity. No in vivo human data were located. Bacterial and limited mammalian assays were negative (Benson et al. 1984; Demerec et al. 1951; Haworth et al. 1983; NTP 1987). Considering the absence of mutation effects in bacterial and mammalian tests evaluating gene mutation and chromosomal aberrations, genotoxicity may not be an area of concern in humans. Based on existing data, additional studies are not needed at this time.
Reproductive Toxicity. No studies were found on the effects of boron compounds on the reproductive system in humans by any route of exposure. Oral studies in animals demonstrated injury to gonads, particularly the testes (Dixon et al. 1979; Lee et al. 1978; NIEHS 1990; Seal and Weeth 1980; Weir and Fisher 1972). No studies were found on chronic dermal and inhalation studies in animals. Sufficient data exist on the potential for boron compounds to affect male reproductive organs in animals (NIEHS 1990; NTP 1987; Weir and Fisher 1972). Data suggest that the severity of effects are species specific (Weir and Fisher 1972). Additional studies would be useful to clarify dose-response relationships. Data suggest the female reproductive system is less susceptible and is affected only at very high dose levels (NIEHS 1990; NTP 1987; Weir and Fisher 1972). Additional studies evaluating reproductive effects in females may not be needed at this time.
Developmental Toxicity. No studies were found on the developmental effects of boron and compounds in humans following inhalation, oral, or dermal exposure. No data are available on the ability of boron to cross the placenta or accumulate in fetal tissue. Studies in rats and mice indicate delayed development and structural defects, primarily in the rib cage, following continuous oral exposure in the diet during pregnancy (Heindel et al. 1991). Existing animal data suggest additional testing would be useful in assessing potential risk to humans.
Immunotoxicity. No studies were found in humans or animals on the effects of boron on the immune system by any route of exposure. Results of chronic studies do not suggest that the immune system is a potential target for boron toxicity. Additional studies are not needed at this time.
Neurotoxicity. Case reports in humans, primarily infants, indicate that neurological effects occur after ingestion of boron at high dose levels (Wong et al. 1964). Degenerative changes in brain cells, perivascular hemorrhage, and intravascular thrombosis have been reported in fatal case reports in infants, but neurochemical or neurophysiological changes have not been reported (Settimi et al. 1982; Wong et al. 1964). No studies are available on neurotoxic effects of boron following inhalation or dermal exposure in humans. Animal data are limited to increased brain enzyme activity (Settimi et al. 1982), but no histopathological data are available. Since data on effects are limited primarily to acute oral exposures at high dose levels, additional studies in animals evaluating other dose levels and exposure durations would be useful in evaluating potential risk to humans who may be exposed to low levels of boron compounds near hazardous waste sites.
Epidemiological and Human Dosimetry Studies. Information exists on the adverse health effects of boron compounds in humans. Studies of workers exposed to boron compounds demonstrated that boron can cause mild irritation of the eyes and respiratory tract (Garabrant et al. 1984, 1985). Other human studies involve case reports of accidental or intentional ingestion of large quantities of boron compounds (Litovitz et al. 1988; Locatelli et al. 1987). The studies identified key health effects (lung, kidney, brain, and liver) associated with boron exposure (Wong et al. 1984). Animal studies indicated the testes as a target tissue. Epidemiological studies of the birth rate of occupationally-exposed workers is currently underway at a major U.S. borate production facility (U.S. Borax and Chemical Corporation 1991).
Biomarkers of Exposure and Effect. Blood and urine borate concentrations are useful biomarkers of exposure (Jansen et al. 1984a; Litovitz et al. 1988). The gastrointestinal tract, skin, and brain are principal target organs following boron exposure in humans. Studies in animals demonstrate that boron compounds can also cause gonadal injury, particularly to the testes (Weir and Fisher 1972). Existing animals studies have established this effect as the most sensitive end point following oral exposure. Studies to determine other biomarkers would be useful in assessing the potential human health risk.
Absorption, Distribution, Metabolism, and Excretion. No quantitative information is available on the absorption, distribution, and metabolism of boron compounds; however, there are studies on the excretion of boron following oral (Jansen et al. 1984a; Litovitz et al. 1988) and inhalation (Wilding et al. 1959) exposures and after dermal exposure (Draize and Kelley 1959). Since data on toxicokinetics of boron are limited, additional studies are needed by all routes of exposure that will provide data on absorption rates, extent of conversion in the body and amount and rate of accumulation in various tissues. Limited data from oral and dermal studies suggest that boron is primarily excreted in urine. Since boron can deposit in the upper respiratory tract, additional excretion studies by this route would be useful in determining if excretion patterns are similar across all routes of exposure.
Comparative Toxicokinetics. Existing evidence from human and animal studies do not indicate whether or not boron compounds affect the same target tissues. Animal studies indicate the testes as a target tissue (Dixon et al. 1979; Lee et al. 1978; NIEHS 1990; Seal and Weeth 1980; Weir and Fisher 1972). Data suggest differences in species sensitivity, with dogs more sensitive than rats and mice (Weir and Fisher 1972). No data have been found on potential reproductive effects of boron and compounds in humans. Data exist on excretion of boron compounds. Based on excretion studies, boron compounds are absorbed by the gastrointestinal tract. There are no available quantitative toxicokinetics data on absorption, distribution, and metabolism. Additional toxicokinetics studies would be useful in assessing differences in species sensitivity, and provide a better basis for extrapolation of animal data to human exposure risk.
Mitigation of Effects. Methods for the mitigation of acute effects of boron poisoning include prevention of absorption of boron from the gastrointestinal tract and standard procedures used to prevent convulsions, severe dehydration or shock (Stewart and McHugh 1990). Saline diuresis, exchange transfusions, peritoneal dialysis, or hemodialysis may be employed to enhance removal of absorbed boron from the body (Goldfrank et al. 1990; Stewart and McHugh 1990). No additional information was located concerning mitigation of effects of lower-level or longer-term exposure to boron. Further information on techniques to mitigate such effects would be useful in determining the safety and effectiveness of possible methods for treating boron-exposed populations in the vicinity of hazardous waste sites.
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