The exponential growth of pollutant discharges into the environment due to increasing industrial and agricultural activities is a rising threat for human health and a biggest concern for environmental health globally. Several synthetic chemicals, categorized as potential environmental endocrine-disrupting chemicals (EDCs), are evident to affect the health of not only livestock and wildlife but also humankind. In recent years, human exposure to environmental EDCs has received increased awareness due to their association with altered human health as documented by several epidemiological and experimental studies. EDCs are associated with deleterious effects on male and female reproductive health; causes diabetes, obesity, metabolic disorders, thyroid homeostasis and increase the risk of hormone-sensitive cancers. Sewage effluents are a major source of several EDCs, which eventually reach large water bodies and potentially contaminate the drinking water supply. Similarly, water storage material such as different types of plastics also leaches out EDCs in drinking Water. Domestic wastewater containing pharmaceutical ingredients, metals, pesticides and personal care product additives also influences endocrine activity. These EDCs act via various receptors through a variety of known and unknown mechanisms including epigenetic modification. They differ from classic toxins in several ways such as low-dose effect, non-monotonic dose and trans-generational effects. This review aims to highlight the hidden burden of EDCs on human health and discusses the non-classical toxic properties of EDCs in an attempt to understand the magnitude of the exposome on human health. Present data on the environmental EDCs advocate that there may be associations between human exposure to EDCs and several undesirable health outcomes that warrants further human bio-monitoring of EDCs.
A cross-sectional study was conducted in 25 spray painters and 35 control subjects to evaluate neurobehavioral function, and thyroid and reproductive hormones profile. This study indicated higher prevalence of psychological and neurological symptoms, and clinical findings among spray painters when compared with controls. Levels of TSH were significantly (p<0.01) elevated in spray painters over the control group (3.04 ± 1.53 vs 1.88 ± 1.07 µ µ µ µ µIU/ml, mean ± SD), respectively.Two of the 25 spray painters acquired sub-clinical hypothyroidism, and one subject was detected with overt hypothyroidism. T 4 levels were significantly (p<0.05) suppressed in spray painters while T 3 was not changed significantly in both the groups. Reproductive hormones (LH, FSH, and testosterone) showed no significant changes in control and spray-painting group. However, two spray painters had abnormally high level of LH (26.43 and 12.22 IU/l; normal range 0.5-10 IU/l). These subjects were also found to have abnormally higher level of FSH (38.63 and 14.11 IU/l; normal range 1.3-11.5 IU/l). An isolated higher level of FSH (39.94 IU/l) was also observed in one spray painter. No abnormality in the level of LH was observed in control group while 3 subjects from this group had abnormally high level of FSH. Testosterone levels were under the normal range (3-12 ng/ ml) in both the groups. This study might suggest that spray painters are at risk of developing neurobehavioral, thyroid and reproductive problems.
The industrial disaster of Bhopal in 1984 resulted into widespread morbidity and mortality in the vicinity of the industry and required long term surveillance for chronic health effects in those affected by the leakage of gas. Although few cytogenetic studies were undertaken to assess genetic damage in survivors of the disaster, no studies are available on cytogenetic damage of toxic gas exposed population having chronic kidney disease (CKD).Thus, the present study aimed to evaluate cytogenetic alterations in chronic kidney disease patients who wereexposed to leaked gas and to compare it with those who were not exposed to the leaked gas. The cytogenetic alterations were evaluated through chromosomal aberration analysis and micronuclei assay. The study included 608 study participants divided into four groups on the basis of history of exposure to the leaked gas and presence or absence of CKD. The results of the study showed no statistically significant difference in cytogenetic damagebetween gas exposed and non-exposed patients of CKD. However, significantly higher cytogenetic damage was observed among gas exposed participants having CKD as compared to gas exposed participants free from CKD.Thus, to conclude though the cytogenetic alterations were observed in exposed group it cannot be solely attributed to the gas exposure and the role of other confounders must also be studied.
The industrial disaster of Bhopal in 1984 resulted in widespread morbidity and mortality in the vicinity of the industry and required long-term surveillance for chronic health effects in those affected by the leakage of gas. Although few cytogenetic studies were undertaken to assess genetic damage in survivors of the disaster, no studies are available on cytogenetic damage of toxic gas-exposed populations having chronic kidney disease (CKD). Thus, the present study aimed to evaluate cytogenetic alterations in chronic kidney disease patients who were exposed to leaked gas and to compare it with those who were not exposed to the leaked gas. The cytogenetic alterations were evaluated through chromosomal aberration analysis and micronuclei assay. The study included 608 study participants divided into four groups based on the history of exposure to the leaked gas and the presence or absence of CKD. The results of the study showed no statistically significant difference in cytogenetic damage between gas-exposed and non-exposed patients of CKD. However, significantly higher cytogenetic damage was observed among gas-exposed participants having CKD as compared to gas-exposed participants free from CKD. Thus, to conclude though the cytogenetic alterations were observed in an exposed group it cannot be solely attributed to the gas exposure and the role of other confounders must also be studied.
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