Environmental Pollutants ; Humans ; Polychlorinated Biphenyls ; Population Surveillance

In this review, we have provided an overview of the environmental risk factors for attention deficit hyperactivity disorder (ADHD), focusing on the major environmental toxicants related to the disorder. Researchers have indicated that since the characteristics of ADHD are complex, the disorder's etiology involves multiple genes of moderate effect interacting with environmental factors. The possible roles of prenatal and perinatal exposure have been the main focus of research on environmental risk factors for ADHD. Among environmental toxicants, we reviewed the potential effects on the development of ADHD of exposure to lead, nicotine, alcohol, polychlorinated biphenyls (PCBs), and dioxin. Further, for the each neurotoxicant, clinical prevention or intervention strategies aimed at reducing a child's risk from environmental toxic insults have been presented.
Attention Deficit Disorder with Hyperactivity ; Nicotine ; Polychlorinated Biphenyls ; Risk Factors

OBJECTIVETo compare the nature of the metabolites formed from the phase I metabolism (hydroxylation and oxidation) and phase II metabolism (glutathionyl conjugation) of PCBs that have different chlorine substitution patterns. To discuss the structure-activity relationships and metabolic mechanisms of PCBs.

METHODS4-Cl-biphenyl (PCB3), 4,4'-Cl-biphenyl (PCB15), 3,4,3',4'-Cl-biphenyl (PCB77) were used for in vitro metabolic study. LC/MS and UV-Vis studies were performed for metabolites identification.

RESULTSThe cytochrome P-450 catalyzed hydroxylation rate decreased as the number of chlorine substitutions increased. In this reaction, PCB3 was fully metabolized, approximately half of the PCB15 was metabolized and PCB77 was not metabolized at all. The oxidation rate of PCB15-HQ was higher than that of PCB3-HQ under various oxidation conditions. The LC/MS and UV-Vis data suggest that in the conjugation reaction of PCB15-Q and GSH, the Michael addition reaction occurs preferentially over the displacement reaction.

CONCLUSIONThe metabolic profiles of polychlorinated biphenyls (PCBs) are dramatically affected by chlorine substitution patterns. It is suggested that the metabolic profiles of PCBs are related to their chlorine substitution patterns, which may have implications for the toxicity of PCB exposure.

PURPOSE: Polychlorinated biphenyls (PCBs, Aroclor 1254), synthetic chlorinated organic compounds, are known to decrease thyroid function, sperm count, and fertility, and increase the risk of testicular cancer; they may have serious effects on male reproduction. The aim of this study was to investigate the possible protective role of palmiwon on PCB-induced spermiotoxicity in rats. MATERIALS AND METHODS: 90-day-old male Sprague Dawley rats were randomly divided into three groups, each consisting of ten animals. The control group (Group I) received corn oil, the second group of rats (Group II) was administered 2 mg/kg body weight/day of Aroclor 1254+corn oil intraperitoneally for 30 days. The third group of rats (Group III) was treated with 2 mg/kg body weight/day of Aroclor 1254+corn oil intraperitoneally plus palmiwon (300 mg/day) orally for 30 days. Twenty-four hours after the last treatment, the animals were killed by decapitation. Their serum testosterone levels was measured before and after the experimental medication was taken, and the number and motility of sperm, which had been collected from the cauda epididymal region, were evaluated. RESULTS: The results of this experiment show that treatment with palmiwon significantly improved sperm motility and number in rats that had been exposed to PCBs. There was no marked difference in body weight, testis weight, or epididymis weight among the groups. Nor were there any significant pathological differences in the testes among the groups. CONCLUSIONS: Palmiwon has the potential for treating PCB-induced spermiotoxicity. More experiments with larger samples and a longer period of treatment are needed.
Animals ; Aroclors ; Biphenyl Compounds ; Body Weight ; Corn Oil ; Decapitation ; Epididymis ; Fertility ; Humans ; Male ; Polychlorinated Biphenyls ; Rats ; Rats, Sprague-Dawley ; Reproduction ; Sperm Count ; Sperm Motility ; Spermatozoa ; Testis ; Testosterone ; Thyroid Gland

Despite the possible consequences of maternal ingestion of polychlorinated biphenyls (PCBs) on future generation, information in limited on how/whether maternal PCB exposure affects testis of the adult male offspring. Therefore, we conducted two experiments to investigate the effects of intermittent and continuous of lactating rats to low and high doses of Aroclor 1242 (a PCB congener) on volume density of seminiferous tubules and interstitium, testis volume, sperm production/day and the total number of Sertoli cells per testis in adult male offspring. In experiment I, 3 groups of lactating Sprague Dawley rats received daily subcutaneous injections of 0.1 ml of corn oil, low dose (8microgram) and high dose (80microgram) of Aroclor 1242 in corn oil respectively, from parturition to weaning of pups at 21 days. In experiment II, 3 groups of lactating rats received 2 subcutaneous injections per week of 0.1 ml corn oil, low and high doses of Aroclor respectively, as in experiment I. Pups in all groups were weaned at day 21 and were raised on a normal diet until sacrificed at 90 days to evaluate volume density of seminiferous tubules and interstitium, testis volume, sperm production/day and the total number of Sertoli cells per testis. Volume density of seminiferous tubules and interstitium per testis was determined by point counting method. Testis volume and sperm production/day was measured by routine techniques. The total number of Sertoli cells per testis was determined by morphometry(disector method). In experiment I and II, the volume density of seminiferous tubules and interstitium per testis was equal in control and treated testes. In experiment I (continuous exposure), the testis volume was increased by 14.8% (low dose)~16.5% (high dose), and sperm production/day and Sertoli cell numbers were increased 20.4~25%, and 32.6~39.4%, respectively. In experiment II (intermittent exposure), testis volume, sperm production/day and the total number of Sertoli cells per testis were not significantly different (p>0.05) in PCB-exposed rats (both low and high doses) compared to controls. It is clear that continuous exposure, but not intermittent exposure of male rats to Aroclor during the neonatalprepubertal period causes detrimental effects on the testis in adult male offspring. These results emphasize the susceptibility of the developing testis to environmental factors during the crucial neonatal period.
Adult* ; Animals ; Aroclors ; Cell Count* ; Corn Oil ; Diet ; Eating ; Humans ; Injections, Subcutaneous ; Male* ; Mothers* ; Parturition ; Polychlorinated Biphenyls* ; Rats* ; Rats, Sprague-Dawley ; Seminiferous Tubules ; Sertoli Cells ; Social Responsibility ; Spermatozoa* ; Testis* ; Weaning

OBJECTIVES: The present subacute study was designed to evaluate the effect of coenzyme Q 10 (CoQ10) in the 28 days aroclor 1254 exposure induced oxidative stress in mice brain. METHODS: Biochemical estimations of brain lipid peroxidation (LPO), reduced glutathione (GSH), and activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and acetyl cholinesterase (AChE), and histopathological investigations of brain tissue were carried out. RESULTS: Oral exposure of aroclor 1254 (5 mg/kg) led to significant decrease in levels of GSH, and activities of SOD, CAT, GPx, and AChE, and increase in LPO. These aberrations were restored by CoQ10 (10 mg/kg, intraperitoneal injection [IP]). This protection offered was comparable to that of L-deprenyl (1 mg/kg, IP) which served as a reference standard. CONCLUSIONS: Aroclor 1254 exposure hampers the activities of various antioxidant enzymes and induces oxidative stress in the brains of Swiss albino mice. Supplementation of CoQ10 abrogates these deleterious effects of aroclor 1254. CoQ10 also apparently enhanced acetyl cholinesterase activity which reflects its influence on the cholinergic system.
Animals ; Aroclors* ; Brain* ; Catalase ; Cats ; Chlorodiphenyl (54% Chlorine)* ; Cholinesterases ; Glutathione ; Glutathione Peroxidase ; Injections, Intraperitoneal ; Lipid Peroxidation ; Methods ; Mice* ; Oxidative Stress ; Selegiline ; Superoxide Dismutase ; Ubiquinone

BACKGROUND: Persistent organic pollutants (POPs) are toxic materials that cannot be broken down naturally and that easily accumulate in the body. Although several studies have attempted to reveal the effects of POPs on the endocrine and nervous system and on cancer, few studies focus on the relationship between low-dose POPs and public health. We attempted to find a relationship between the level of POPs and common gastrointestinal symptoms, including abdominal discomfort, diarrhea, and constipation. METHODS: We recruited 121 subjects who visited Kyungpook National University Hospital for a health screening. Plasma concentrations were evaluated for 40 kinds of POPs including 17 types of polychlorinated biphenyls and 23 types of organochlorine pesticides. Furthermore, the Korean version of the Rome III criteria was used to identify gastrointestinal symptoms. RESULTS: Our results showed that abdominal discomfort had an inverse relationship with several polychlorinated biphenyls. Moreover, an inverted U-shaped relationship was observed between abdominal discomfort and several other organochlorine pesticides including p,p'-dichlorodiphenyldichloroethane and p,p'-dichlorodiphenyltrichloroethane, and the effects of these pesticides on abdominal discomfort were similar to that of organochlorine pesticides on obesity and metabolic syndrome. CONCLUSION: Our results suggest that mild and unspecified gastrointestinal symptoms with no clear cause could be related to POPs levels.
Constipation ; Diarrhea ; Gyeongsangbuk-do ; Mass Screening ; Nervous System ; Obesity ; Pesticides ; Plasma ; Polychlorinated Biphenyls ; Public Health

For the previous century, the humans have created an unintended and unwanted problem of endocrine disruptors as a potential threat to our public health. By the name of industrialization, endocrine disruptors are smuggling in the everyday life of people today. Although there are much debate on the reality of their emerging health threat, it is no doubt that there are certain classes of compounds that have the potential to affect hormonal status adversely, leading to abnormal development, reproductive dysfunction, and some cancers. The classes of endocrine disruptors are extensively diverse and even more increasing, such as, polychlorinated biphenyls (PCBs), dioxins, dieldrin, bisphenol A and toxaphene. Although these endocrine disruptors have been prohibited or tightly regulated, many of them are still unrecognized and still used without knowing their potential threat to the biological world. Once they are released into the environment, they usually persist without degradation and even undergo bioaccumulation and bioconcentration in food chain. Comparing with the great concern over the public health, we do not have enough information for these issues. It is now clear that we need further extensive studies for the risk assessment and the protection of human and ecological health from the potential hazards of endocrine disruptors. This article introduces a breif overview of the current status of our knowledge and research on endocrine disruptors.
Dieldrin ; Dioxins ; Endocrine Disruptors* ; Food Chain ; Humans ; Polychlorinated Biphenyls ; Public Health ; Risk Assessment ; Toxaphene

Chloracne is a refractory acneiform eruption due to halogenated polyaromatic compound(eg. dioxin, dibenzofurans, polychlorinated biphenyls, etc.). 2, 3, 7, 8-tetrachlorodibenzo-p-dioxin, a kind of dioxin isomer, contained in the Agent Orange which was used for defoliating agent during Vietnam war. It is characterized by recalcitrant comedones and cyst predominantly in the malar and postauricular area. Lesions of the penis and scrotum are also relatively frequent. The key pathological feature is the non-inflammatory keratinization of pilosebaceous unit. The meibomian glands are typically affected. Xerosis, conjunctivitis, pigmentation, follicular hyperkeratosis, actinic elastosis are occasionally associated with chloracne. We report a case of typical chloracne due to exposure to defoliating agent during Vietnam war in a 54-year-old-man who shows typical clinical and histopathological features.
Acneiform Eruptions ; Actins ; Chloracne* ; Citrus sinensis ; Conjunctivitis ; Male ; Meibomian Glands ; Penis ; Pigmentation ; Polychlorinated Biphenyls ; Scrotum ; Vietnam*

OBJECTIVETo study the effect of polychlorinated biphenyl, Aroclor1254 on benzo (a) pyrene [B (a) P]-induced DNA damage in HepG2 cells.

METHODSHepG2 cells were pretreated with Aroclor1254 (11.5, 23 and 46 micromol/L) for 24 hours and then exposed to B (a) P (50 micromol/L). DMSO (10 ml/L) was used as solvent control. Single cell gel electrophoresis (SCGE) and high-performance liquid chromatography-electrochemical detection (HPLC-EC) assays were applied to detect DNA single-strand breaks and 8-hydroxy-2'-deoxyguanosine (8-OHdG) in HepG2 cells, respectively.

RESULTSAverage Oliver tail moment (OTM) and 8-OHdG level in HepG2 cells were significantly increased in B (a) P treated group (1.66 +/- 0.21), (23.31 +/- 6.02) 8-OHdG/10(6)dG than that in solvent control (0.79 +/- 0.15), (12.31 +/- 3.24) 8-OHdG/10(6)dG, respectively. In Aroclor 1254 treated group (11.5, 23.0, 46.0 micromol/L), average OTM were 0.88 +/- 0.20, 1.01 +/- 0.15 and 1.10 +/- 0.16, and 8-OHdG levels were (19.57 +/- 7.57), (22.80 +/- 9.16) and (31.74 +/- 9.25) 8-OHdG/10(6)dG, respectively. A concentration of 46 micromol/L Aroclor1254 caused a significant increase of 8-OHdG level as compared with the solvent control. After pretreatment of HepG2 cells with Aroclor1254 (11.5, 23.0 and 46.0 micromol/L), B (a) P induced more DNA strand breaks (OTM: 2.14 +/- 0.22, 2.43 +/- 0.32 and 2.71 +/- 0.31) and 8-OHdG [(32.50 +/- 3.81), (49.23 +/- 16.66) and (60.36 +/- 18.04) 8-OHdG/10(6)dG] in HepG2 cells than B (a) P alone.

CONCLUSIONAroclor1254 might enhance B (a) P-induced DNA damage in HepG2 cells, which should imply a synergistic effect of Aroclor1254 on the genotoxicity of B (a) P.