Reproductive toxicity kidney effects

Target organs of chloroform toxicity are the central nervous system, liver, and kidneys (see Section 2.2). Respiratory, cardiovascular, and gastrointestinal toxic effects have also been reported. Studies in animals also indicated that chloroform exposure may induce reproductive and developmental effects and cause cancer. Several studies investigated the possible mechanism for chloroform-induced toxicity (see Section 2.5). Proposed mechanisms of chloroform toxicity and potential mitigations based on these mechanisms are discussed below. The potential mitigation techniques mentioned are all experimental. 

Reproductive toxicity to 2,3,7,8-TCDD has been demonstrated in animals. "" The effects include pre- and postimplantation losses in females, morphologic and functional changes in male and female reproductive organs, and hormonal imbalance in both sexes. A number of developmental effects have been observed in animals acutely exposed to 2,3,7,8-TCDD by the oral route. Effects observed in offspring of animals include cleft palate, kidney anomalies, immune system damage (thymic atrophy and immunosuppression), impaired development of the reproductive system, decreased growth, and fetal/newborn mortality. 

Reproductive toxicity was observed in rats administered lOOmg/kg by gavage in a continuous breeding protocol experiment fewer Fi pups were born live, and lower Fi pup weights and higher Fi pup mortality were observed. Increased liver and kidney weights were found at necropsy. These effects occurred at levels that also produced systemic toxicity, suggesting that dicyclopentadiene is not selectively a reproductive toxin. 

Reproductive Toxicity. No data are available on the reproductive toxicity of hexachlorobutadiene in humans. Hexachlorobutadiene did not cause adverse reproductive effects in mice or rats after inhalation or oral exposures, even at dose levels causing kidney and liver damage (Harleman and Seinen 1979 Kociba etal. 1977a NIOSH 1981 NTP 1991 Saillenfait et al. 1989 Schwetzetal. 1977). No data are available on the reproductive toxicity of hexachlorobutadiene after dermal exposure. Based on existing data in animals, it does not appear that exposure to the compound would pose any significant risk to human reproduction. 

Chronic exposures to lead by inhalation or the oral route cause adverse effects that include damage to the peripheral and central nervous system, anemia, and chronic kidney damage. Lead accumulates in the soft tissues and bones, with the highest accumulation in the liver and kidneys, and elimination is slow. Lead has shown developmental and reproductive toxicity in both male and female... 

SAFETY PROFILE Poison by intravenous and subcutaneous routes. Moderately toxic by ingestion and intraperitoneal routes. An experimental teratogen. Human systemic effects by ingestion and intraperitoneal routes change in vestibular functions, blood pressure decrease, eosinophilia, respiratory depression, and pulmonary changes. Human reproductive and teratogenic effects by unspecified routes developmental abnormalities of the eye and ear and effects on newborn including postnatal measures or effects. Toxic to kidneys and central nervous system. Has been implicated in aplastic anemia. Experimental reproductive effects. Human... 

The health-effects data on JP-8 and related fuels were reviewed for the following end points respiratory tract toxicity, neurotoxicity, immunotoxicity, liver toxicity, kidney toxicity, reproductive and developmental toxicity, cardiovascular toxicity, genotoxicity, and carcinogenicity. JP-8 was found to be potentially toxic to the immune system, respiratory tract, and nervous system at exposure concentrations near the interim PEL of350 mg/m3. Those toxicides are summarized below. 

Additional research on cadmium is recommended in three areas (1) effects on cancer, genotoxicity, and reproductive toxicity under conditions of acute, intermediate, and chronic durations of exposure, and administered by way of diet, iiflialation, and dermal routes of exposure (2) emphasis on studies with pregnant animals and (3) methods for reducing toxic effects. Finally, the issue of the significance of cadmium residues in various body parts requires resolution. At this time, it appears that cadmium residues in the vertebrate kidney or liver that exceed... 

Other toxic effects observed due to PAHs include decrease body weight, enlarged liver with cell edema and congestion of the liver parenchyma, reproductive toxicities, destruction of oocytes, and inflammation of kidney cells [15]. Developmental toxicities such as embryolethality, reduced fetal weight, and malformations have been reported in response to benz[fl]anthracene, benzo[a]pyrene, dibenz[fl,lt]anthracene, and naphthalene [13,16]. A series of studies have been conducted on the reproductive and developmental toxicity in humans. These were carried out in several countries such as Ukraine [17], United States [18], and Czech Republic [19]. Even though these studies did not have enough data to conclude a correlation, results from the numerous studies on laboratory animals indicate so. 

While there is some evidence that exposure to NP or OP may have adverse effects on specific organs, including the kidney, heart, and liver, the majority of the studies evaluating toxic effects of APs have focused on male and female reproduction and endocrine effects, immune function, and neurological and behavioral endpoints. This section will briefly highlight some of the studies that have assessed effects of AP exposure on these organs and functional systems, especially those from mammalian laboratory animal models and tissue culture systems. 

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