Reproductive toxic potential of phthalate compounds - State of art review.

Phthalates are pervasive compounds, and due to the ubiquitous usage of phthalates, humans or even children are widely exposed to them. Since phthalates are not chemically bound to the plastic matrix, they can easily leach out to contaminate the peripheral environment. Various animal and human studies have raised vital health concern including developmental and reproductive toxicity of phthalate exposure. The present review is based upon the available literature on phthalates with respect to their reproductive toxic potential. Common reproductive effects such as declined fertility, reduced testis weight, variations in accessory sex organs and several female reproductive disorders appeared to be largely associated with the transitional phthalates. Among the higher molecular weight phthalates (≥ C7), di-isononyl phthalate (DINP) produces some minor effects on development of male reproductive tract and among low molecular weight phthalates (≤C3), di-methyl (DMP) and di-isobutyl (DIBP) phthalate produce some adverse effects on male reproductive system. Whereas transitional phthalates such as di-butyl phthalate, benzyl butyl phthalate, and di-(2-ethylhexyl) phthalate have shown adverse effects on female reproductive system. Owing to these, non-toxic alternatives to phthalates may be developed and use of phthalates could be rationalized as an important issue where human reproduction system is involved. Though, more epidemiological studies are needed to substantiate the reported findings on phthalates.

Occupational and environmental mercury exposure and human reproductive health - a review.

Mercury is a toxic heavy metal. Humans are exposed to mercury through several sources including environmental, occupational, contaminated food and water and from mercury-containing dental amalgam. Mercury exposure is known to harm the nervous system profoundly, and have a negative impact on digestive and immune systems, and other organs. To review and discuss the effect of mercury exposure through environmental or occupational routes on human reproduction, pregnancy, and its outcome. Published information about the potential toxic effects of mercury on human reproduction were collected and summarized. Literature was identified by systematic search using relevant keywords. Literature review revealed a number of negative impacts of mercury on human reproduction. These included effects on semen quality, including reduced sperm count, motility, and changes in morphology that may reduce fertility potential. There may also be an effect in changing reproductive hormone levels. Mercury exposure might also affect pregnancy but the data concerning mercury effects on female reproduction are limited except for some data about mercury exposure and poor pregnancy outcomes. Available data indicate that mercury exposure may have a toxicity effect on reproductive potential, especially in males. Prenatal mercury exposure may affect pregnancy or its outcome and this appears to be dependent upon dose, duration, and timing of exposure. Nutritional status of exposed individual might also influence the impact of mercury.

Role of Oxidative Stress in Male Reproductive Dysfunctions with Reference to Phthalate Compounds.

PURPOSE: A wide variety of environmental chemicals/xenobiotics including phthalates have been shown to cause oxidative stress targeting the endocrine system and cause reproductive anomalies. The present review describes various issues by oxidative stress causing male reproductive dysfunctions. Here in this review, the importance and role of phthalate compounds in male reproductive dysfunction has been well documented. MATERIALS AND METHODS: One class of environmental endocrine disruptors is phthalates. Phthalate compounds are mostly used as plasticizers, which increase the flexibility, durability, longevity, and etc. of the plastics. Large-scale use of plastic products in our daily life as well as thousands of workers engaged in the manufacture of plastic and plastic products and recycling plastic industry are potentially exposed to these chemicals. Further, general population as well as vulnerable groups i.e. children and pregnant women are also exposed to these chemicals. Phthalates are among wide variety of environmental toxicants capable of compromising male fertility by inducing a state of oxidative stress in the testes. They may also generate reactive oxygen species (ROS) that may affect various physiological and reproductive functions. RESULTS: The available data points out that phthalate compounds may also induce oxidative stress in the male reproductive organs mainly testis and epididymis. They impair spermatogenic process by inducing oxidative stress and apoptosis in germ cells or target sertoli cells and thereby hamper spermatogenesis. They also impair the Leydig cell function by inducing ROS, thereby decreasing the levels of steroidogenic enzymes. CONCLUSION: Thus in utero and postnatal exposure to phthalate compounds might lead to decreased sperm count and various other reproductive anomalies in the young male.

Determination of in vivo estrogenic potential of Di-isobutyl phthalate (DIBP) and Di-isononyl phthalate (DINP) in rats.

Estrogenic potential of Di-isobutyl phthalate (DIBP) and Di-isononyl phthalate (DINP) was studied using two different test systems. Two different doses of DIBP (250 and 1250 mg/kg) and DINP (276 and 1380 mg/kg) were administered to immature female rats (20 days old) orally once daily for 3 and 20 days in uterotrophic and pubertal assay, respectively. The animals were sacrificed on day 4 and day 41 in case of 3-day uterotrophic and 20-day pubertal assay, respectively. The results indicated that non-significant alterations in uterine and ovarian wet weight were observed in both the DIBP- and DINP-treated groups while the uterus weight increased significantly (i.e., 4-6 times) in the Diethylstilbesterol (DES)-treated group in both the assays. In the present study, precocious vaginal opening occurred at 26 days of age in the DES-treated group with a mean body weight of 30.39 ± 1.08 g. However, no precocious vaginal opening was found in any of the DIBP- and DINP-treated groups. The results indicated that both the phthalate compounds were unable to induce elevation in the uterine weight in both the assays and unable to cause vaginal opening indicating non-estrogenic potential of both the phthalate compounds, i.e., DIBP and DINP in vivo.