Influence of the drinking water disinfection by-product dibromoacetic acid on rat estrous cyclicity and ovarian follicular steroid release in vitro

Balchak, Sharon K.; Hedge, Joan M.; Murr, Ashley S.; Mole, M. Leonard; Goldman, Jerome M.

doi:10.1016/s0890-6238(00)00104-0

Cited by 22 publications

(10 citation statements)

References 21 publications

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“…No adverse effects on female reproductive performance or development of the female offspring were associated with exposure to concentrations of DBA as high as 650 ppm. Thus, ndings of altered estrous cycling reported in rats using gavage oral dosages of 90 and 270 mg/kg/day (Balchak et al 2000) were not observed in this study using drinking water as the mode of exposure, possibly because the high levels of exposure attained by the gavage route versus the drinking water route were not attained. The reported reduction in primordial follicles in rabbits (Bodensteiner et al 2001) also was not observed in the rats in this study.…”

Section: Figurecontrasting

confidence: 61%

“…Female rats given DBA by gavage at dosages of 0 to 270 mg/kg/day for 14 days and evaluated for estrous cyclicity during treatment and for 2 weeks post treatment identi ed dosedependent alterations in cyclicity at 90-and 270-mg/kg/day dosages (Balchak et al 2000). These alterations persisted after completion of treatment in the 270-mg/kg/day dosage group.…”

Section: Female Reproductive Effectsmentioning

confidence: 99%

“…In a subsequent in vitro assessment by these authors (Balchak et al 2000), the in uence of DBA on steroid release was examined. Mean blood levels of DBA were determined over a 5-hour period following an oral (gavage) dosage of 270 mg/kg/day.…”

Section: Female Reproductive Effectsmentioning

confidence: 99%

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Oral (Drinking Water) Two-Generation Reproductive Toxicity Study of Dibromoacetic Acid (DBA) in Rats

et al. 2002

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In a two-generation study of dibromoacetic acid (DBA), Crl SD rats (30 rats/sex/group/generation) were provided DBA in drinking water at 0 (reverse osmosis-deionized water), 50, 250, and 650 ppm (0, 4.4 to 11.6, 22.4 to 55.6, and 52.4 to 132.0 mg/kg/day, respectively; human intake approximates 0.1 microg/kg/day [0.0001 mg/kg/day]). Observations included viability, clinical signs, water and feed consumption, body and organ weights, histopathology, and reproductive parameters (mating, fertility, abortions, premature deliveries, durations of gestation, litter sizes, sex ratios and viabilities, maternal behaviors, reproductive organ weights, sperm parameters and implantation sites, sexual maturation). Histopathological evaluations were performed on at least 10 P and F1 rats/sex at 0 and 650 ppm (gross lesions, testes, intact epididymis; 10 F1 dams at 0, 250, and 650 ppm for primordial follicles). Developmental observations included implantations, pup numbers, sexes, viabilities, body weights, morphology, and reproductive performance. At 50 ppm and higher, both sexes and generations had increased absolute and relative liver and kidneys weights, and female rats in both generations had reduced absolute and relative adrenal weights; adrenal changes were probably associated with physiological changes in water balance. The livers and kidneys (10/sex/group/generation) had no histopathological changes. Other minimal effects at 50 ppm were reduced water consumption and a transient reduction in body weight. At 250 and 650 ppm, DBA reduced parental water consumption, body weight gains, body weights, feed consumption, and pup body weights. P and F1 generation male rats at 250 and 650 ppm had altered sperm production (retained step 19 spermatids in stages IX and X tubules sometimes associated with residual bodies) and some epididymal tubule changes (increased amounts of exfoliated spermatogenic cells/residual bodies in epididymal tubules, atrophy, and hypospermia), although inconsistently and at much lower incidences. Unilateral abnormalities of the epididymis (small or absent epididymis) at 650 ppm in four F1 generation male rats were considered reproductive tract malformations. The no-observable-adverse-effect level (NOAEL) and reproductive and developmental NOAELs for DBA were at least 50 ppm (4.5 to 11.6 mg/kg/day), 45,000 to 116,000 times the human adult exposure level. Reproductive and developmental effects did not occur in female rats exposed to DBA concentrations as high as 650 ppm. Based on the high multiples of human exposure required to produce effects in male rats, DBA should not be identified as a human reproductive or developmental risk.

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Section: Figurecontrasting

confidence: 61%

Section: Female Reproductive Effectsmentioning

confidence: 99%

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Oral (Drinking Water) Two-Generation Reproductive Toxicity Study of Dibromoacetic Acid (DBA) in Rats

et al. 2002

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“…27, 28 In addition, dibromoacetic acid disrupts estrous cyclicity and suppresses estradiol catabolism, which leads to alterations in steroid production in female rats. 29, 30 …”

Section: Introductionmentioning

confidence: 99%

Monohaloacetic acid drinking water disinfection by-products inhibit follicle growth and steroidogenesis in mouse ovarian antral follicles in vitro

Jeong

Gao

Dettro

et al. 2016

Reproductive Toxicology

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Water disinfection greatly reduced the incidence of waterborne diseases, but the reaction between disinfectants and natural organic matter in water leads to the formation of drinking water disinfection by-products (DBPs). DBPs have been shown to be toxic, but their effects on the ovary are not well defined. This study tested the hypothesis that monohalogenated DBPs (chloroacetic acid, CAA; bromoacetic acid, BAA; iodoacetic acid, IAA) inhibit antral follicle growth and steroidogenesis in mouse ovarian follicles. Antral follicles were isolated and cultured with either vehicle or DBPs (0.25–1.00 mM of CAA; 2–15 µM of BAA or IAA) for 48 and 96 h. Follicle growth was measured every 24 h and the media were analyzed for estradiol levels at 96 h. Exposure to DBPs significantly inhibited antral follicle growth and reduced estradiol levels compared to controls. These data demonstrate that DBP exposure caused ovarian toxicity in vitro.

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“…Experimental, animal, and epidemiologic studies provide evidence that a number of these DBPs, including trihalomethanes, may be associated with adverse pregnancy outcomes (Balchak et al 2000; Bove et al 2002; Gemma et al 2003; Goldman and Murr 2002; Plewa et al 2004; Ward et al 2000). However, epidemiologic studies exploring the effect of drinking water chlorination and total trihalomethane (TTHM) exposures on preterm birth in human populations have reported equivocal results.…”

mentioning

confidence: 99%

Estimated Effects of Disinfection By-products on Preterm Birth in a Population Served by a Single Water Utility

Lewis

Suffet

Hoggatt

et al. 2007

Environ Health Perspect

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ObjectivesWe evaluated the association between drinking-water disinfection by-products and preterm births using improved exposure assessment and more appropriate analysis methods than used in prior studies.MethodsDuring 1999–2001, vital record data were obtained for a large, racially diverse population residing in 27 Massachusetts communities that received drinking water from a single public utility. This water system was monitored weekly for total trihalomethanes (TTHM), and it maintained geographically stable total TTHM levels system-wide during the study period. We employed proportional hazards regression to examine the effects of trimester-specific and shorter-term peak exposures to TTHM in drinking water late in pregnancy on preterm births in 37,498 singletons.ResultsFor all women, our data suggested no more than a small increase, if any, in risk for delivering a preterm baby when exposed to ≥ 60 μg/L TTHM during the 4 weeks before birth [hazard ratio (HR) = 1.13; 95% confidence interval (CI), 0.95–1.35]. However, women who depended on a governmental source of payment for prenatal care were at increased risk when exposed at such levels late in gestation (HR = 1.39; 95% CI, 1.06–1.81). In contrast, exposure to high levels of TTHM during the second trimester and high exposure throughout pregnancy resulted in a 15–18% reduction in risk for preterm delivery in our population.ConclusionsThis finding confirms previous reports of a negative association during the second trimester. Our data also suggested a possible positive association with shorter-term third-trimester TTHM exposure in mothers of lower socioeconomic status.

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Influence of the drinking water disinfection by-product dibromoacetic acid on rat estrous cyclicity and ovarian follicular steroid release in vitro

Cited by 22 publications

References 21 publications

Oral (Drinking Water) Two-Generation Reproductive Toxicity Study of Dibromoacetic Acid (DBA) in Rats

Oral (Drinking Water) Two-Generation Reproductive Toxicity Study of Dibromoacetic Acid (DBA) in Rats

Monohaloacetic acid drinking water disinfection by-products inhibit follicle growth and steroidogenesis in mouse ovarian antral follicles in vitro

Estimated Effects of Disinfection By-products on Preterm Birth in a Population Served by a Single Water Utility

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