The objectives of this study were to determine the effects of prolonged exposure to perchlorate on (1) thyroid status and reproductive performance of adult zebrafish (Danio rerio) and (2) F1 embryo survival and early larval development. Using a static-renewal procedure, mixed sex populations of adult zebrafish were exposed to 0, 10, and 100 mg/l nominal concentrations of waterborne perchlorate for 10 weeks. Thyroid histology was qualitatively assessed, and females and males were separated and further exposed to their respective treatments for six additional weeks. Eight females in each tank replicate (n = 3) were paired weekly with four males from the same respective treatment, and packed-egg (spawn) volume (PEV) was measured each of the last five weeks. At least once during weeks 14–16 of exposure, other end points measured included fertilization rate, fertilized egg diameter, hatching rate, standard length, and craniofacial development of 4-day–postfertilization larvae and thyroid hormone content of 3.5-h embryos and of exposed mothers. At 10 weeks of exposure, perchlorate at both concentrations caused thyroidal hypertrophy and colloid depletion. A marked reduction in PEV was observed toward the end of the 6-week spawning period, but fertilization and embryo hatching rates were unaffected. Fertilized egg diameter and larval length were increased by parental exposure to perchlorate. Larval head depth was unaffected but the forward protrusion of the lower jaw–associated cartilage complexes, Meckel's and ceratohyal, was decreased. Exposure to both concentrations of perchlorate inhibited whole-body thyroxine content in mothers and embryos, but triiodothyronine content was unchanged. In conclusion, prolonged exposure of adult zebrafish to perchlorate not only disrupts their thyroid endocrine system but also impairs reproduction and influences early F1 development.

Cyanobacteria are the most common toxigenic algae in inland waters. Their toxins can affect the health of aquatic and terrestrial organisms, including humans. Other algal groups, such as haptophytes (e.g., Prymnesium parvum) and euglenoids (e.g., Euglena sanguinea), can also form harmful algal blooms (HABs) whose toxins cause injury to aquatic biota but currently have no known effects on human health. Prymnesium parvum, however, is responsible for some of the worst HAB-related ecological disasters recorded in inland waters. Here, we provide an overview of the primary toxigenic algae found in U.S. inland waters: cyanobacteria (planktonic forms), P. parvum, and E. sanguinea with the objective of describing their similarities and differences in the areas of HAB ecology, algal toxins, and the potential for future range expansion of HABs. A detailed account of bloom habitats and their known associations with land cover and use is provided from the perspective of water quality. This review revealed that salinity may have an influence on inland cyanobacterial blooms and cyanotoxins that had not been fully recognized previously.

Perchlorate inhibits iodide uptake by thyroid follicles and lowers thyroid hormone production. Although several effects of perchlorate on the thyroid system have been reported, the utility of these pathologies as markers of environmental perchlorate exposures has not been adequately assessed. The present study examined time‐course and concentration‐dependent effects of perchlorate on thyroid follicle hypertrophy, colloid depletion, and angiogenesis; alterations in whole‐body thyroxine (T₄) levels; and somatic growth and condition factor of subadult and adult zebrafish. Changes in the intensity of the colloidal T₄ ring previously observed in zebrafish also were examined immunohistochemically. Three‐month‐old zebrafish were exposed to ammonium perchlorate at measured perchlorate concentrations of 0, 11, 90, 1,131, and 11,480 ppb for 12 weeks and allowed to recover in clean water for 12 weeks. At two weeks of exposure, the lowest‐observed‐effective concentrations (LOECs) of perchlorate that induced angiogenesis and depressed the intensity of colloidal T₄ ring were 90 and 1,131 ppb, respectively; other parameters were not affected (whole‐body T₄ was not determined at this time). At 12 weeks of exposure, LOECs for colloid depletion, hypertrophy, angiogenesis, and colloidal T₄ ring were 11,480, 1,131, 90, and 11 ppb, respectively. All changes were reversible, but residual effects on angiogenesis and colloidal T₄ ring intensity were still present after 12 weeks of recovery (LOEC, 11,480 ppb). Whole‐body T₄ concentration, body growth (length and weight), and condition factor were not affected by perchlorate. The sensitivity and longevity of changes in colloidal T₄ ring intensity and angiogenesis suggest their usefulness as novel markers of perchlorate exposure. The 12‐week LOEC for colloidal T₄ ring is the lowest reported for any perchlorate biomarker in aquatic vertebrates.