A two-generational reproductive toxicity study of zinc in rats

A two-generation reproductive toxicity study of zinc chloride (ZnCl₂) was conducted in rats. F_o male and female rats were administered 0.00 (control), 7.50 (low), 15.00 (mid) and 30.00 (high) mg/kg/day of ZnCl₂. Selected F₁ male and female rats were exposed to the same doses received by their parents (F_o). Exposure of F₀ parental rats to ZnCl₂ showed significant reduction in fertility, viability (days 0 and 4), and the body weight of F₁ pups from the high-dose group but caused no effects on litter size, weaning index, and sex ratio. Similarly, the continued exposure of F₁ parental rats to ZnCl₂ also reduced fertility, liter size, viability (day 0), and the body weight of F₂ pups within the high-dose group but caused no effects on weaning index and sex ratio. Exposure of ZnCl₂ to F₀ and F₁ parental males resulted in a significant reduction in their body weights, and the F₀ and F₁ parental females did not show any significant difference in their body weights compared to their control groups. However, the postpartum dam weights of both F₀ and F₁ female rats were significantly reduced compared to their controls. Exposure of ZnCl₂ to F_o and F₁ generation parental rats did not produce any significant change of their clinical signs as well as their clinical pathology parameters, except the alkaline phosphotase (ALK) level, which showed an upward trend in both sexes of both generations. Exposure of ZnCl₂ to F₀ rats resulted in a reduction of brain, liver, kidney, spleen and seminal vesicles weights of males and in the spleen and uterus of females. Similarly, exposure of F₁ rats to ZnCl₂ also resulted in reduction of brain, liver, kidney, adrenal, spleen, prostate and seminal vesicles weights of males and in spleen and uterus of females. ZnCl₂ exposure resulted in grossly observed gastro-intestianla (GI) tract, lymphoreticular/hematopoietic, and reproductive tract lesions in parental rats in both generations. Reduced body fat was also recorded in F₁ parental rats.     

Brain myelination in rats treated with ionizing radiation in utero

Abstract

Effects of ionizing radiation on brain myelination and some physical development parameters were studied in laboratory rats (Fisher F‐344 inbred strain). Rats were treated with three different doses of radiation (150 rad, 15 rad, and 6.8 rad) delivered on the 20th day of prenatal life. Exposure to 150 rad reduced body, brain, ovary, kidney, heart and spleen weights. Prenatal exposure to 150 rad of radiation reduced the cerebral cortex weight by 22 percent at 30 days of age, and 20 percent at 52 days of age which caused a reduction in cerebral cortex myelin content by 20 and 23 percent at the ages of 30 and 52 days respectively. This dose did not affect the myelin content of the cerebellum or the brain stem, or the myelin concentration (mg myelin/g brain tissue) of the cerebral cortex, cerebellum, and the brain stem. The cerebral cortex weight of the 15 rad treated rats was reduced at the age of 30 days. Exposure to 15 rad, and 6.8 rad did not affect either the myelin content or the myelin concentration of these brain areas.     

Brain myelination in rats treated with ionizing radiation in utero.

Effects of ionizing radiation on brain myelination and some physical development parameters were studied in laboratory rats (Fisher F-344 inbred strain). Rats were treated with three different doses of radiation (150 rad, 15 rad, and 6.8 rad) delivered on the 20th day of prenatal life. Exposure to 150 rad reduced body, brain, ovary, kidney, heart and spleen weights. Prenatal exposure to 150 rad of radiation reduced the cerebral cortex weight by 22 percent at 30 days of age, and 20 percent at 52 days of age which caused a reduction in cerebral cortex myelin content by 20 and 23 percent at the ages of 30 and 52 days respectively. This dose did not affect the myelin content of the cerebellum or the brain stem, or the myelin concentration (mg myelin/g brain tissue) of the cerebral cortex, cerebellum, and the brain stem. The cerebral cortex weight of the 15 rad treated rats was reduced at the age of 30 days. Exposure to 15 rad, and 6.8 rad did not affect either the myelin content or the myelin concentration of these brain areas.     

Toxicological response and its reversibility in rats fed Lake Ontario or Pacific coho salmon for 13 weeks

Lake Ontario coho salmon were known to contain a mixture of chemical contaminants. A previous study demonstrated that rats fed the Lake Ontario fish-supplemented diet for 28 days exhibited mild biochemical and histological changes. The purpose of the present study was to determine the effects due to a longer term of exposure and the reversibility of these effects. Growth rate and food consumption were not affected by feeding the animals with Lake Ontario or Pacific fish-supplemented diets for 13 weeks. No deaths were observed. Decreased spleen weights were observed in groups of males fed 1.45%, 5.8% Lake Ontario and 2.9% Pacific diet. After a 13 week recovery the spleen weights returned to normal. Decreased serum potassium was observed in male rats fed 2.9% Lake Ontario diet, and all levels of Pacific diet for 13 weeks, and was not evident following maintenance on normal diet. Serum glucose was not affected by the 13-week period of treatment, however; a reduction in this parameter occurred in male rats fed the two highest doses of Lake Ontario diet and all doses of Pacific diet following the 13-week recovery period. Minor hematological changes occurred only in the male rats fed either Lake Ontario or Pacific diet following a 13 week recovery period and included reduced marrow myeloid cells and myeloid/erythroid ratio. Hepatic microsomal ethoxyresorufin deethylase activity was significantly increased in rats ingesting Lake Ontario diet. Mild histological changes occurred in the liver and thyroid of the treated males, and in the liver and kidney of the treated females. These changes were attributed to the chemical residues and/or the fish diet. Data presented here indicated that the Lake Ontario fish-supplemented diet can cause mild biochemical, hematological and histological changes but most of these were reversible when exposure was terminated.     

Toxicological response and its reversibility in rats fed Lake Ontario or pacific coho salmon for 13 weeks

Abstract

Lake Ontario coho salmon were known to contain a mixture of chemical contaminants. A previous study demonstrated that rats fed the Lake Ontario fish‐supplemented diet for 28 days exhibited mild biochemical and histological changes. The purpose of the present study was to determine the effects due to a longer term of exposure and the reversibility of these effects. Growth rate and food consumption were not affected by feeding the animals with Lake Ontario or Pacific fish‐supplemented diets for 13 weeks. No deaths were observed. Decreased spleen weights were observed in groups of males fed 1.45%, 5.8% Lake Ontario and 2.9% Pacific diet. After a 13 week recovery the spleen weights returned to normal. Decreased serum potassium was observed in male rats fed 2.9% Lake Ontario diet, and all levels of Pacific diet for 13 weeks, and was not evident following maintenance on normal diet. Serum glucose was not affected by the 13‐week period of treatment, however; a reduction in this parameter occurred in male rats fed the two highest doses of Lake Ontario diet and all doses of Pacific diet following the 13‐week recovery period. Minor hematological changes occurred only in the male rats fed either Lake Ontario or Pacific diet following a 13 week recovery period and included reduced marrow myeloid cells and myeloid/erythroid ratio. Hepatic microsomal ethoxyresorufin deethylase activity was significantly increased in rats ingesting Lake Ontario diet. Mild histological changes occurred in the liver and thyroid of the treated males, and in the liver and kidney of the treated females. These changes were attributed to the chemical residues and/or the fish diet. Data presented here indicated that the Lake Ontario fish‐supplemented diet can cause mild biochemical, hematological and histological changes but most of these were reversible when exposure was terminated.     

Effect of cadmium on ATPase activities in rats fed on iron-deficient and sufficient diets

Male Sprague-Dawley rats were fed on different levels of cadmium mixed with purified diets containing iron or no iron for 8 weeks. The body weight gain, tissue weights, hemoglobin, hematocrit, liver and brain ATPase were measured at 2, 4 and 8 weeks after feeding. The hemoglobin and hematocrit values were the same in all rats fed on cadmium. The rats fed on iron-deficient diets mixed with cadmium showed a significant decrease in body weight gain. However, the rats receiving only the 100 ppm of cadmium in iron-sufficient diet showed a significant decrease in body weight gain. There were no significant changes in the weights of thymus, spleen, kidney, heart, brain and testes. However, the liver weights were decreased in the highest treatment of cadmium but the liver weight/body ratios were uneffected. Na+-K+ activated ATPase activity in brains of rats fed on cadmium were significantly decreased at 2, 4 and 8 weeks of treatment. The decrease was more pronounced in rats fed on iron-deficient diets. Oligomycin-sensitive (Mitochondrial) Mg2+ ATPase activity was also significantly decreased in liver and brain tissues of rats fed on cadmium. Oligomycin-insensitive Mg2+ ATPase activity, however, was not altered in any tissues tested. It appears that cadmium may be interfering with energy (ATP) production and utilization processes in rat brain and liver tissues.     

The induction of metallothionein in tissues of the Norway lobster Nephrops norvegicus following exposure to cadmium, copper and zinc: the relationships between metallothionein and the metals

Nephrops norvegicus were exposed simultaneously to cadmium, copper and zinc over an 18-day period. Exposure concentrations were control, 1, 5 and 25 microg litre(-1) for cadmium and copper and 8, 40 and 200 microg litre(-1) for zinc. Concentrations of cadmium, copper, zinc and metallothionein were measured in homogenates of both the gill and the hepatopancreas. Quantification of metallothionein was carried out by differential pulse polarography. Cadmium concentrations increased significantly in the gill and hepatopancreas of both male and female animals in response to increases in exposure concentration. In contrast, the concentration of copper and zinc increased significantly in the gills of males, but not in females. In the hepatopancreas, neither copper nor zinc resulted in significant changes in concentrations of these metals. Metallothionein concentrations in the gill and hepatopancreas were increased significantly in relation to metal exposure in both males and females. Concentrations of cadmium and metallothionein in both the gill and hepatopancreas of males and females were positively correlated. Copper in the hepatopancreas also showed positive relationships with MT concentrations in males, but not in females. This study suggested that cadmium MTs in the gill and hepatopancreas of Nephrops norvegicus could be used as a sensitive tool to detect cadmium contamination in the lobsters, although this was not true for copper and zinc.     

Toxicological assessment of chlorinated diphenyl ethers in the rat

Chlorinated diphenyl ethers are environmental contaminants that have been found in Great Lakes fish and birds. Because of their presence in the food chain, and potential for human exposure, the present short-term study was conducted to assess their toxicity. Groups of 10 male and 10 female rats were each given by gavage 2,2',4,4'6-pentachlorodiphenyl ether (CDE1), 2,2',4,4',5,6-hexachlorodiphenyl ether (CDE2) or 2,2',3,3',4,6'-hexachlorodiphenyl ether (CDE3) at dose levels of 0.04, 0.4, 4.0 or 40 mg/kg b.w./day for a period of 28 days. The control group received an equivalent volume of corn oil only (0.5 ml/100 g b.w.). Treatment with the three CDE congeners did not result in suppression of growth rate or food consumption. Increased liver weights were seen in the animals of both sexes fed 40 mg/kg CDE2, in males treated with 40 mg/kg CDE1, and in females with 40 mg/kg CDE3. Hepatic microsomal aminopyrine demethylase activity was significantly higher in the male rats administered 40 mg/kg CDE2, and aniline hydroxylase activity was elevated in the females following the same treatment. Serum glucose, calcium, protein and urea nitrogen of CDE1-treated males were higher than the control. Levels of uric acid, potassium and LDH of CDE3-treated females were also elevated. No hematological changes were observed. Histological examination revealed that the liver and thyroid were the target organs affected by CDE treatment but the morphological changes were mild even at the highest dose level. Changes in the liver consisted of nuclear vesiculation and increased cytoplasmic volume. Alterations in the thyroid were characterized by increased epithelial height and follicular collapse. Based on the data presented above, the 3 CDE congeners can only be considered moderately toxic in the rat.     

Impacts of weathered tire debris on the development of Rana sylvatica larvae

Highway runoff has the potential to negatively impact receiving systems including stormwater retention ponds where highway particulate matter can accumulate following runoff events. Tire wear particles, which contain about 1% Zn by mass, make up approximately one-third of the vehicle derived particulates in highway runoff and therefore may serve as a stressor to organisms utilizing retention ponds as habitat. In this study, we focused on the potential contribution of tire debris to Zn accumulation by Rana sylvatica larvae and possible lethal or sublethal impacts resulting from exposure to weathered tire debris during development. Eggs and larvae were exposed to aged sediments (containing either ZnCl2 or tire particulate matter, both providing nominal concentrations of 1000 mg Zn kg(-1)) through metamorphosis. Water column Zn was elevated in both the ZnCl2 and tire treatments relative to the control treatment, indicating that aging allowed Zn leaching from tire debris to occur. Tissue Zn was also elevated for the ZnCl2 and tire treatments indicating that Zn in the treatments was available for uptake by the amphibians. Exposure to both ZnCl2 and tire treatments increased the time for larvae to complete metamorphosis in comparison with controls. We also observed that the longer the organisms took to complete metamorphosis, the smaller their mass at metamorphosis. Our results indicate that Zn leached from aged tire debris is bioavailable to developing R. sylvatica larvae and that exposure to tire debris amended sediments can result in measurable physiological outcomes to wood frogs that may influence population dynamics.     

The subchronic toxicity of acridine in the rat

Abstract

The subchronic toxicity of acridine was investigated in rats following dietary exposure at 0, 1, 10, 100 and 500 ppm for 13 weeks. The growth rate and food consumption were not affected by treatment and no clinical signs of toxicity were observed. There was a slight but significant decrease in spleen weight, both in absolute terms and as a percent of body weight, in the 500 ppm males and a slight increase in absolute thymus weight in the females of the same dose group. Both hepatic ethoxyresorufin O‐deethylase (EROD) and pentoxyresorufin O‐dealkylase (PROD) activities were slightly, but significantly, elevated in females in the 500 ppm dose group. No haematological or other biochemical changes were observed. Females also displayed dose‐related increases in inorganic phosphate and uric acid levels. Treatment‐related histopathological changes were seen in the thyroid, liver and kidney and included hepatic anisokaryosis and vesiculation of nuclei and glomerular adhesions, reticulin sclerosis and nuclear pyknosis in the kidney. Residue data showed a dose‐dependent accumulation of acridine in liver, kidney and adipose with the highest concentration being found in the fat of the 500 ppm dose group. Based on these data, the no observable adverse effect level of acridine was judged to be 100 ppm or 12 mg/kg bw/day.     

Induction of rat hepatic microsomal enzymes by toxaphene pretreatment

Abstract

The effects of pretreatment of rats with toxaphene on hepatic drug metabolizing enzymes and several other parameters of the mixed function oxidase system were investigated. Adult male Sprague‐Dawley rats were fed diets containing 0, 50, 100, 150 and 200 ppm of toxaphene for 14 days. The body weight gain was unaltered as well as the food consumption in all the toxaphene fed groups. There was no change in the weights of brain, kidney, heart, and testes but the liver weight was significantly increased. The thymus weight in all the toxaphene fed groups was decreased. Hydroxylation of pentobarbital and aniline was significantly enhanced in rats exposed to toxaphene. Ethylmorphine‐N‐demethy‐lase activity in the toxaphene treated rats was also elevated. Enhanced hydroxylation of pentobarbital was also evident from the decreased sleeping time following pentobarbital administration. Exposure to toxaphene increased cytochrome P‐450, NADPH‐cytochrome c‐reductase and dehydrogenase in hepatic microsomal fractions. The binding of aniline and hexobarbital to microsomes was also enhanced, suggesting that the intermediate steps in the electron‐transfer system were increased. In conclusion, pretreatment of rats with toxaphene for fourteen days resulted in the induction of the hepatic mixed function oxidase system.     

Low doses of chlorpyrifos interfere with spermatogenesis of rats through reduction of sex hormones

Use of pesticides results in indirect effects on human health. We aimed to evaluate implications of toxicological effects of subchronic chlorpyrifos exposure on reproductive function in male rats. A total of 48 adult Wistar male rats were separated into four groups (n = 12). Animals were gavaged with 2.5 mg/kg (T1), 5 mg/kg (T2), or 10 mg/kg (T3) body weight of chlorpyrifos (CPF) or distilled water (control) daily for 30 days. Organ weights, epididymal sperm parameters, DNA integrity, sex hormonal (FHS and LH) levels, and alanine aminotransferase (ALT), aspartate aminotransferase (AST), gamma-glutamyl transferase (GGT), and creatinine concentrations were determined on day 31. Another two sets of (four groups/set; n = 10) animals were orally treated with the same doses of CPF, control animal groups were treated with distilled water only for 30 days, and fertility indices and blood plasma acetylcholine esterase (AchE) were determined on day 31. Exposure to CPF resulted in a significant (p < 0.05) decrease in weights of testis and epididymis. An increase in liver weight resulted in reduced sperm counts and sperm motility and an increase in sperm abnormalities. Significant reduction in serum testosterone (p < 0.01), luteinizing hormone (p < 0.05), and follicular stimulating hormone (p < 0.05) levels was evident in animals treated with the highest dose. A significant decrease in the number of viable implantation sites and pups was observed in female rats mated with the T3 (p < 0.01) and T2 (p < 0.05) males. The ALT, AST, GGT, and creatinine contents were significantly increased (p < 0.05 and p < 0.01, respectively) on CPF exposure. A significant (p < 0.01) reduction in blood plasma AchE enzyme was observed with the highest dose. Our results demonstrated that prolonged exposure of CPF induces spermatogenesis damage, possibly through interference with sex hormones and AchE enzyme resulting in reduction of fertility. Therefore, awareness programs on handling CPF (pesticides) to enhance safety warrant minimization of its hazards.     

Toxicological assessment of chlorinated diphenyl ethers in the rat

Abstract

Chlorinated diphenyl ethers are environmental contaminants that have been found in Great Lakes fish and birds. Because of their presence in the food chain, and potential for human exposure, the present short‐term study was conducted to assess their toxicity. Groups of 10 male and 10 female rats were each given by gavage 2,2’,4,4'6‐pentachlorodiphenyl ether (CDE1), 2,2’,4,4’,5,6‐hexachlorodiphenyl ether (CDE2) or 2,2’,3,3’,4,6'‐hexachlorodiphenyl ether (CDE3) at dose levels of 0.04, 0.4, 4.0 or 40 mg/kg b.w./day for a period of 28 days. The control group received an equivalent volume of corn oil only (0.5 ml/100 g b.w.). Treatment with the three CDE congeners did not result in suppression of growth rate or food consumption. Increased liver weights were seen in the animals of both sexes fed 40 mg/kg CDE2, in males treated with 40 mg/kg CDE1, and in females with 40 mg/kg CDE3. Hepatic microsomal aminopyrine demethylase activity was significantly higher in the male rats administered 40 mg/kg CDE2, and aniline hydroxylase activity was elevated in the females following the same treatment. Serum glucose, calcium, protein and urea nitrogen of CDE1‐treated males were higher than the control. Levels of uric acid, potassium and LDH of CDE3‐treated females were also elevated. No hematological changes were observed. Histological examination revealed that the liver and thyroid were the target organs affected by CDE treatment but the morphological changes were mild even at the highest dose level. Changes in the liver consisted of nuclear vesiculation and increased cytoplasmic volume. Alterations in the thyroid were characterized by increased epithelial height and follicular collapse. Based on the data presented above, the 3 CDE congeners can only be considered moderately toxic in the rat.     

Two formulations of the industrial surfactant, Toximul, differentially reduce mouse weight gain and hepatic glycogen in vivo during early development: effects of exposure to Influenza B Virus

Previous studies demonstrated that young mice exposed chronically to industrial surfactant (IS) do not exhibit obvious adverse health effects, but do have persistently reduced body weights and compromised hepatic energy metabolism. The present study examined the time course of effects of two formulations of the Toximul (Tox) class of anionic/nonionic IS on body weights and liver glycogen (+/-virus) during early development. Results showed that effects differed in two commonly used strains of mice. In CFW mice, 12 days' exposure to Tox resulted in retardation of weight gain that was most obvious several days after exposure ceased. In this strain effects were greater with Tox 3409F than with Tox MP-A and appeared to be reversible except when the mice were treated with both Tox 3409F and FluB. Weights of the CD-1 mice were not affected by either Tox treatment alone, but were significantly reduced on postnatal day 20 when Tox exposure had been combined with FluB infection. Postnatal replenishment of hepatic glycogen stores during the first three weeks also occurred at different rates in CFW and CD-1 mice. The effects of Tox (+/-FluB) on glycogen also varied with mouse strain and Tox formulation. In CFW mice, exposure to either formulation resulted in significant (55-59%) reductions in glycogen, although reductions were not evident until nine days after Tox exposure stopped. By contrast, hepatic glycogen in CD-1 mice was reduced both during and after dermal exposure to Tox 3409F, whereas no effect was observed with Tox MP-A. Notably, the 3409F effect was reversible in the CD-1 mice, but reversal did not occur in mice also infected with FluB. Tox MP-A+FluB-treated mice exhibited only a transient glycogen reduction. These results illustrate the importance of mouse strain and formulation specificities in assessing biological effects of xenobiotic surfactants. As well, they emphasize that chronic IS exposure can induce changes in growth and energy substrate availability in young mice that may not be evident unless there is a precipitating cofactor such as a viral infection.     

Splenocyte apoptotic pathway in mice following oral exposure to cerium trichloride

With their widespread application in agriculture, industry, culture, medicine, and daily life, lanthanide compounds are being brought into the ecological environment and human body through food chains. It is important to know the acute and chronic effects of lanthanides on the environment, nature balance, and the human body after their entry into bodies and the environment. Lanthanides have been demonstrated to cause spleen apoptosis and decreased immunity of mice, but very little is known about the molecular aspects of these mechanism. In order to understand the spleen apoptotic mechanism induced by intragastric administration of 2, 10 and 20 mg kg(-1) body weight CeCl(3) for consecutive 60 d, we investigated the cerium accumulation, apoptosis, the expression levels of the apoptosis-related cytokines into apoptosis-related genes and proteins. The results demonstrated that cerium had obvious accumulation in the mouse spleen, leading to the significant increase of the spleen indices and splenocyte apoptosis. Furthermore, CeCl(3) could effectively activate caspase-3 and -9, decrease the Bcl-2 the levels of gene and protein, and increase the levels of Bax, and cytochrome c genes and their protein expressions, and promote reactive oxygen species production. It implied CeCl(3)-induced apoptosis in the mouse spleen via intrinsic pathway. Our findings suggest the need for great caution to handle the lanthanides for workers and consumers.     

Dietary exposure to technical hexabromocyclododecane (HBCD) alters courtship, incubation and parental behaviors in American kestrels (Falco sparverius)

Hexabromocyclododecane (HBCD) is a high production volume brominated flame retardant that has been detected in the environment and wildlife at increasing concentrations. This study was designed to determine potential effects of dietary exposure to environmentally relevant levels of HBCD on behavior during reproduction in captive American kestrels. Twenty kestrel pairs were exposed to 0.51 μg technical HBCD g⁻¹ kestrel d⁻¹ from 4 weeks prior to pairing until chicks hatched (∼75 d). Ten pairs of controls received the safflower oil vehicle only and were used for comparison. During the courtship period the chitter-calls were reduced in both sexes (p = 0.038) and females performed fewer bonding displays (p = 0.053). Both sexes showed a propensity to be less active than controls during courtship. The reduction in male courtship behavior was correlated with reduced courtship behaviors of females (p ? 0.008) as well as reduced egg mass (p = 0.019). During incubation, nest temperatures of treatment pairs were lower at mid-incubation (p = 0.038). HBCD-exposed males performed fewer key parental behaviors when rearing nestlings, including entering the nest-box, pair-bonding displays and food-retrievals. HBCD-exposed females appeared to compensate for the reduced parental behavior of their mates by performing these same behaviors more frequently than controls (p = 0.004, p = 0.027, p = 0.025, respectively). This study demonstrates that HBCD affects breeding behavior in American kestrels throughout the reproductive season and behavioral alterations were linked to reproductive changes (egg size). This is the first study to report HBCD effects on reproductive behavior in any animal model.     

Residues of persistent organic pollutants in frequently-consumed vegetables and assessment of human health risk based on consumption of vegetables in Huizhou,South China

Concentrations of 16 polycyclic aromatic hydrocarbons (PAHs), 16 phthalate esters (PAEs), eight organochlorine pesticides (OCPs) and seven polychlorinated biphenyls (PCBs) in 17 frequently-consumed varieties of vegetables collected from 48 sites in Huizhou were measured. Concentrations of PAHs and PAEs of leafy vegetables were higher than those of gourd and fruit vegetables but it was the opposite for OCPs and PCBs. A questionnaire of 450 local residents on vegetable consumption showed that the total vegetable ingested rates of females and males were 278.80 g person⁻¹ d⁻¹ and 282.92 g person⁻¹ d⁻¹, respectively. The weight-specific daily intakes of pollutants by females were higher than those by males because of differences in body weight. Twenty-seven pollutants were used to assess the potential risk to human health by calculating target hazard quotient (THQ) values. Results showed that the risk to females was higher than for males. OCPs were the major contributors to the risk for both females and males. The main risks were from consumption of eggplant, Chinese lettuce and luffa and were significantly related to the contents of di-nonyl phthalate, β-hexachlorocyclohexane, γ-hexachlorocyclohexane, p,p-dichlorodiphenyltrichloroethane and p,p-dichlorodiphenyl dichloroethane in vegetables. Although the THQ values induced by individual pollutants were relatively low, the total THQ values induced by 27 pollutants were above 1 in some administrative regions of Huizhou, which might give cause for concern.     

In vitro assessment of the effects of cadmium and zinc on mammalian nerve fibres

Zinc and cadmium are environmental contaminants that have a wide range of effects on the nervous system, but zinc is also considered to be an important metal in the human body. In this study the effect of CdCl(2) and ZnCl(2), at concentrations of 50,150, 250 and 500 microM, on the nerve fibres of the sciatic nerve of the rat isolated in a three-chamber recording bath were studied. At the same concentrations, CdCl(2) and ZnCl(2) were found to have almost the same inhibitory effect on the compound action potential (CAP) of the nerve fibres. Their concentration-effect curves almost overlap and there was no significant difference in their EC(50) which for CdCl(2) is 250.1+/-18 microM (n=5) and for ZnCl(2) is 282.2+/-25 microM (n=5) correspondingly (P>0.05). The no-observed-effect concentration (NOEC) was estimated to be 50-100 microM for both metals. The identical inhibitory effect of both metals on the sciatic nerve fibres indicates a common mode of action which is related to their potential to generate reactive oxygen species (ROS).     

Age trends and reproductive transfer of organochlorine compounds in long-finned pilot whales from the Faroe Islands

Total DDT and PCB concentrations were determined in blubber of 130 long-finned pilot whales, Globicephala melas (100 females and 30 males) from the Faroe Islands (northern north-east Atlantic). In males and immature females no relation was observed between age and organochlorine concentrations or the ratio of tDDT (total DDT)/PCB; in contrast, concentrations and ratios in mature females declined with age, which is attributed to reproductive transfer to their offspring during gestation and lactation. Relative abundance of DDE respective to tDDT increased in males and young females and decreased in mature females. Organochlorine transfer to offspring during lactation was found to represent about 60-100% of the mother's body load, while that occurring during gestation was estimated to be much lower, in the range 4-10% of mother's body load. Transfer rates tended to decrease with mother's age and were, consequently, much higher in primiparous females than in those that had already given birth. Transplacental rates were found to be consistent with the ratio between mother's body weight and neonatal body weight.