2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) Toxicity during Early Life Stage Development of Lake Trout (Salvelinus namaycush)

1991 ◽  
Vol 48 (5) ◽  
pp. 875-883 ◽  
Author(s):  
Mary K. Walker ◽  
Jan M. Spitsbergen ◽  
James R. Olson ◽  
Richard E. Peterson
Keyword(s):  
Adverse Effect ◽  
Lake Trout ◽  
Life Stage ◽  
Early Life Stage ◽  
Salvelinus Namaycush ◽  
Yolk Sac ◽  
Adverse Effect Level ◽  
Effect Level ◽  
Life Stage Development ◽  
Related Mortality

Lake trout (Salvelinus namaycush) eggs containing [3H]TCDD concentrations from 0 to 302 parts per trillion (ppt) were observed through the fry stage for TCDD metabolism, elimination, and toxicity. All radioactive residues extracted from eggs and sac fry were due to TCDD; no metabolites were detected. [3H]TCDD was not eliminated from eggs and sac fry, but was rapidly eliminated from fry (t1/2, 35–37 d). Hatchability was less at egg TCDD concentrations [Formula: see text]; however, the greatest TCDD-related mortality occurred during the sac fry stage. In all TCDD groups (34–302 ppt), sac fry that died developed subcutaneous yolk sac edema prior to death, resembling blue-sac disease. The development of yolk sac edema preceded sac fry mortality, and the severity of edema varied directly with cumulative mortality. Based on TCDD concentrations in the egg resulting from a 48-h exposure, the no observable adverse effect level (NOAEL) for mortality was 34 ppt and the lowest observable adverse effect level (LOAEL) was 55 ppt. The TCDD concentration in eggs that caused 50% mortality above control at swim-up (LD50) was 65 ppt. Lake trout sac fry exposed as eggs are more sensitive to the lethal effects of TCDD than any mammalian, avian, or fish species investigated thus far.

Translocation of 2,3,7,8-Tetrachlorodibenzo-p-dioxin from Adult Female Lake Trout (Salvelinus namaycush) to Oocytes: Effects on Early Life Stage Development and Sac Fry Survival

1994 ◽  
Vol 51 (6) ◽  
pp. 1410-1419 ◽  
Author(s):  
Mary K. Walker ◽  
Philip M. Cook ◽  
Allan R. Batterman ◽  
Brian C. Butterworth ◽  
Christine Berini ◽  
...  
Keyword(s):  
Lake Trout ◽  
Life Stage ◽  
Early Life Stage ◽  
Salvelinus Namaycush ◽  
Mature Female ◽  
Wet Weight ◽  
Stage Development ◽  
Tetrachlorodibenzo P Dioxin ◽  
Life Stage Development ◽  
Sexually Mature

There were no signs of overt toxicity in sexually mature female lake trout (Salvelinus namaycush) exposed to either a control or a 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-containing diet for 11 wk prior to spawning. At spawning the maternally derived egg TCDD concentrations were 42 ± 4 and 43 ± 6% of the maternal skeletal muscle TCDD concentration on a lipid and wet weight basis, respectively. Egg TCDD concentrations of 233–387 pg TCDD/g egg (wet weight) resulted in nonviable oocytes, while concentrations of 50–152 pg/g resulted in a dose-related increase in sac fry mortality associated with yolk sac edema, craniofacial alterations, and arrested development, resembling blue-sac disease. The dose–response relationship for sac fry mortality associated with blue-sac disease was essentially identical to that observed when fertilized lake trout eggs were exposed to either waterborne or injected TCDD. The no and lowest observable adverse effect levels for sac fry mortality were 23 and 50 pg/g (maternal egg exposure), 34 and 40 pg/g (waterborne egg exposure), and 44 and 55 pg/g (egg injection). LD50s, based on egg TCDD concentration, were 58 (36–90), 69 (64–75), and 80 (68–91) pg/g (95% fiducial limits) following egg exposure via maternal, waterborne, or injection routes, respectively.

Early Life Stage Mortality Syndrome in Fishes of the Great Lakes and Baltic Sea

1998 ◽  
Keyword(s):  
Baltic Sea ◽  
Salmo Salar ◽  
Early Life ◽  
Life Stage ◽  
Early Life Stage ◽  
Mortality Rates ◽  
Yolk Sac ◽  
The Mean ◽  
The Baltic ◽  
Related Mortality

<em>Abstract</em>.—Since 1974, feral salmon <em>Salmo salar </em>populations of the Baltic Sea have suffered from a yolk sac fry mortality known as the M74 syndrome. Mortality rates of 40–95% have been recorded during the 1990s in compensatory rearing stations along the east coast of Sweden. The M74 syndrome has been linked to the offspring of specific females and associated with low thiamine (vitamin B<sub>1</sub>) concentrations in both female tissues and their progeny. This study evaluated the effect of thiamine treatments on mortality and thiamine concentrations in progeny with and without M74. Eggs and newly hatched yolk sac fry were immersed in water containing thiamine at concentrations of 100, 500, or 2,000 mg/L. Hardening of eggs in water containing thiamine at 500 or 2,000 mg/L completely eliminated M74-related mortality, whereas treatment with thiamine at 100 mg/L only partially reduced M74 mortality. The mean thiamine concentrations at the yolk sac fry stage (21–23 d after hatching) in untreated normal and M74-affected groups were between 0.70–1.0 and 0.19–0.26 nmol/g, respectively. At the same sampling, the mean thiamine concentrations in groups in which eggs were waterhardened in thiamine at 500 or 2,000 mg/L were between 0.8 and 9.4 times higher than the concentrations in the untreated groups. A thiamine threshold limit interval of 0.34–0.47 nmol/g was estimated for the development of M74 in yolk sac fry.

Selective Vulnerability of Dopaminergic Systems To Industrial Chemicals: Risk Assessment of Related Neuroendocrine Changes

1998 ◽  
Vol 14 (1-2) ◽  
pp. 311-323 ◽  
Author(s):  
Antonio Mutti ◽  
Audrey Smargiassi
Keyword(s):  
Adverse Effect ◽  
Selective Vulnerability ◽  
Common Finding ◽  
Serum Prolactin ◽  
Industrial Chemicals ◽  
Limit Values ◽  
Reference Limit ◽  
Individual Level ◽  
Adverse Effect Level ◽  
Effect Level

Increased serum prolactin (PRL) is a common finding among subjects exposed to styrene, perchloroethylene, lead (Pb), and manganese (Mn) at levels below the current threshold limit values. On a group basis, abnormally high basal PRL shows a dose-related distribution among workers exposed to styrene, Pb, and Mn. On the basis of dose-response relationships, the benchmark doses (BMD) for styrene metabolites in urine, lead in blood (Pb-B), and Mn in urine (Mn-U), are 4 mg/g creatinine, 112 μg/L, and 0.3 μg/L, respectively. Noteworthy, the BMD for Mn-U and Pb-B is well below the upper reference limit. A shift in the distribution but not in the prevalence of abnormally high values of serum PRL was observed among perchloroethylene-exposed dry cleaners, which makes interpretation in terms of risk difficult. The measurement of PRL thus provides opportunities for early identification of excess exposure to neurotoxic chemicals affecting dopaminergic control of pituitary secretion. For styrene, Pb, and Mn the BMD provides an objective and statistically determined threshold, which seems to be in good agreement with the estimated no-observed-adverse-effect-level (NOAEL). The NOAEL, however, is based on traditional approaches that require the application of uncertainty factors, e.g., a default factor of 10 when extrapolating the NOAEL from the lowest-observed- adverse-effect-level (LOAEL). Due to its sensitivity to a number of potential confounders, caution must be exercised when using PRL as a screening test at the individual level. Also, age and sex dependent variations in susceptibility may hamper extrapolations from the occupational settings to the general population.

scholarly journals Vitamin D deficiency serves as a precursor to stunted growth and central adiposity in zebrafish

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Megan M. Knuth ◽  
Debabrata Mahapatra ◽  
Dereje Jima ◽  
Debin Wan ◽  
Bruce D. Hammock ◽  
...  
Keyword(s):  
Vitamin D ◽  
Vitamin D Deficiency ◽  
Early Life ◽  
Life Stage ◽  
Somatic Growth ◽  
Early Life Stage ◽  
Cytokine Signaling ◽  
Central Adiposity ◽  
Stage Development ◽  
Life Stage Development

Abstract Emerging evidence demonstrates the importance of sufficient vitamin D (1α, 25-dihydroxyvitamin D3) levels during early life stage development with deficiencies associated with long-term effects into adulthood. While vitamin D has traditionally been associated with mineral ion homeostasis, accumulating evidence suggests non-calcemic roles for vitamin D including metabolic homeostasis. In this study, we examined the hypothesis that vitamin D deficiency (VDD) during early life stage development precedes metabolic disruption. Three dietary cohorts of zebrafish were placed on engineered diets including a standard laboratory control diet, a vitamin D null diet, and a vitamin D enriched diet. Zebrafish grown on a vitamin D null diet between 2–12 months post fertilization (mpf) exhibited diminished somatic growth and enhanced central adiposity associated with accumulation and enlargement of visceral and subcutaneous adipose depots indicative of both adipocyte hypertrophy and hyperplasia. VDD zebrafish exhibited elevated hepatic triglycerides, attenuated plasma free fatty acids and attenuated lipoprotein lipase activity consistent with hallmarks of dyslipidemia. VDD induced dysregulation of gene networks associated with growth hormone and insulin signaling, including induction of suppressor of cytokine signaling. These findings indicate that early developmental VDD impacts metabolic health by disrupting the balance between somatic growth and adipose accumulation.

scholarly journals Lowest observed adverse effect level of pulmonary pathological alterations due to nitrous acid exposure in guinea pigs

2020 ◽  
Vol 25 (1) ◽  
Author(s):  
Masayuki Ohyama ◽  
Hiroshi Nishimura ◽  
Kenichi Azuma ◽  
Chika Minejima ◽  
Norimichi Takenaka ◽  
...  
Keyword(s):  
Adverse Effect ◽  
Smooth Muscle ◽  
Electron Microscope ◽  
Epithelial Cells ◽  
Guinea Pigs ◽  
Pulmonary Emphysema ◽  
Nitrous Acid ◽  
Bronchial Epithelial ◽  
Adverse Effect Level ◽  
Effect Level

Abstract Background We previously demonstrated that continuous exposure to nitrous acid gas (HONO) for 4 weeks, at a concentration of 3.6 parts per million (ppm), induced pulmonary emphysema-like alterations in guinea pigs. In addition, we found that HONO affected asthma symptoms, based on the measurement of respiratory function in rats exposed to 5.8 ppm HONO. This study aimed to investigate the dose-response effects of HONO exposure on the histopathological alterations in the respiratory tract of guinea pigs to determine the lowest observed adverse effect level (LOAEL) of HONO. Methods We continuously exposed male Hartley guinea pigs (n = 5) to four different concentrations of HONO (0.0, 0.1, 0.4, and 1.7 ppm) for 4 weeks (24 h/day). We performed histopathological analysis by observing lung tissue samples. We examined samples from three guinea pigs in each group under a light microscope and measured the alveolar mean linear intercept (Lm) and the thickness of the bronchial smooth muscle layer. We further examined samples from two guinea pigs in each group under a scanning electron microscope (SEM) and a transmission electron microscope (TEM). Results We observed the following dose-dependent changes: pulmonary emphysema-like alterations in the centriacinar regions of alveolar ducts, significant increase in Lm in the 1.7 ppm HONO-exposure group, tendency for hyperplasia and pseudostratification of bronchial epithelial cells, and extension of the bronchial epithelial cells and smooth muscle cells in the alveolar duct regions. Conclusions These histopathological findings suggest that the LOAEL of HONO is < 0.1 ppm.

1,1,2,2-Tetrafluoroethane (HFC-134) (2018)

2019 ◽  
Vol 35 (3) ◽  
pp. 196-203
Keyword(s):  
Adverse Effect ◽  
Adverse Effects ◽  
Toxicity Study ◽  
Whole Body ◽  
Exposure Level ◽  
Inhalation Toxicity ◽  
Hfc 134A ◽  
Adverse Effect Level ◽  
Effect Level ◽  
Whole Body Inhalation

1,1,2,2-Tetrafluoroethane (HFC-134) is a colorless gas used as a foam expansion agent and heat transfer fluid. HFC-134 has a low acute inhalation toxicity with an LC50 of >244,000 ppm. The no-observed adverse effect level (NOAEL) and lowest-observed adverse effect level for cardiac sensitization (in epinephrine-challenged beagle dogs) were 75,000 and 100,000 ppm, respectively. A subacute 4-week GLP inhalation toxicity study exposed male and female Crl: CD®BR rats (10/sex) to 0, 2000, 10,000, or 50,000 ppm via whole-body inhalation. Transient and non-dose-response–related body weight changes were observed throughout the exposure period, but no statistically significant, test substance-related adverse effects were observed in any clinical observations, chemistry, hematology, or pathology. This study identified a NOAEL for HFC-134 of 50,000 ppm, the highest exposure level tested. HFC-134 is not genotoxic in in vitro studies; however, no in vivo studies are available. No developmental or maternal toxicity was found in female rats exposed to HFC-134 up to 50,000 ppm via whole-body inhalation in two different studies. Based on data for a similar material (HFC-134a), HFC-134 is not expected to be extensively metabolized or to cause genetic toxicity or carcinogenicity. The HFC-134 workplace environmental exposure level (WEEL) is based primarily on the subacute 4-week inhalation toxicity study in rats with the NOAEL of 50,000 ppm selected as the point of departure for the derivation of the 8-h TWA, health-based WEEL value. The developmental toxicity study also had a NOAEL of 50,000 ppm and was the highest exposure level tested. The subacute inhalation NOAEL was adjusted to account for interindividual variability, subacute to chronic duration, animal to human extrapolation, daily duration of exposure, and residual uncertainty. In addition, the lack of adverse effects noted in the toxicology studies for HFC-134a was considered. The resulting 8-h TWA WEEL value of 1000 ppm is expected to provide a significant margin of safety against the production of any potential adverse health effects in workers following long-term inhalation exposure to HFC-134.

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