Low-level environmental lead exposure may accelerate progressive renal insufficiency in patients without diabetes who have chronic renal disease. Repeated chelation therapy may improve renal function and slow the progression of renal insufficiency.

The novel anti-inflammatory therapy reduces the mortality rate for patients with severe paraquat poisoning.

Abstract. Previous retrospective research suggests that lowlevel environmental lead exposure is associated with an acceleration of age-related impairment of renal function. For elucidating the long-term relationship between low-level environmental lead exposure and progression of chronic renal diseases in patients without diabetes, 121 patients who had chronic renal insufficiency, a normal body lead burden (BLB), and no history of exposure to lead were observed prospectively for 48 mo. Associations of both BLB and blood lead level (BLL) with renal function were evaluated, with reference to other covariates. The primary end point was an increase in the serum creatinine level to double the baseline value. Sixty-three patients had BLB Ն80 g and Ͻ600 g (high-normal group), and 58 patients had BLB Ͻ80 g (low-normal group). The primary end point occurred in 17 patients. Fifteen of them had high-normal BLB, whereas two patients had low-normal BLB (hazard ratio [95% confidence interval]: 1.01 [1.00 to 1.01] for each increment of 1 g; P ϭ 0.002). The BLB and BLL at baseline were the most important risk factors to predict progression of renal insufficiency. Each increase of 10 g in the BLB or 1 g/dl in the BLL reduced the GFR by 1.3 (P ϭ 0.002) or 4.0 ml/min (P ϭ 0.01) during the study period. In conclusion, low-level environmental lead exposure is associated with accelerated deterioration of renal insufficiency. Even at levels far below the normal ranges, both increased BLL and BLB predict accelerated progression of chronic renal diseases.A high occupational lead exposure is well documented to be able to induce nephropathy (1,2). Several studies have indicated a strong association between blood lead levels (BLL) and agerelated decline in renal function of the general population (3-6). However, these studies either were retrospective or did not adjust other confounding factors that affect the progression of renal function, such as hypertension, urinary protein excretion, and usage of angiotensin-converting enzyme (ACE) inhibitors.Furthermore, most of these studies measured BLL as an indicator of lead exposure. However, the BLL reflects recent lead exposure rather than the actual body lead burden (BLB). Calcium disodium EDTA mobilization tests and bone x-ray fluorescence studies are the most reliable methods for measuring the BLB (7). A BLB of Ͼ600 g (2.9 mol), as assessed by calcium disodium EDTA mobilization tests, indicates lead poisoning. The authors' previous studies, using EDTA-mobilization tests to assess the BLB, suggested that low-level environmental lead exposure may be associated with the progression of renal insufficiency in patients without known lead exposure (8 -10). Our recent work further established that repeated chelation therapy to reduce the BLB may slow the progression of renal insufficiency in a 27-mo clinical trial (11). However, the long-term relationship between low-level environmental lead exposure and the progression of chronic renal diseases remains unknown. A 48-mo prospective longitudinal stu...

Repeated pulses of CP and MP, rather than high doses of CP and DEX, may result in a lower mortality rate in patients with severe PQ poisoning.

IntroductionParaquat poisoning is characterized by multi-organ failure and pulmonary fibrosis with respiratory failure, resulting in high mortality and morbidity. The objective of this study was to identify predictors of mortality in cases of paraquat poisoning. Furthermore, we sought to determine the association between these parameters.MethodsA total of 187 patients were referred for management of intentional paraquat ingestion between January 2000 and December 2010. Demographic, clinical, and laboratory data were recorded. Sequential organ failure assessment (SOFA) and acute kidney injury network (AKIN) scores were collected, and predictors of mortality were analyzed.ResultsOverall hospital mortality for the entire population was 54% (101/187). Using a multivariate logistic regression model, it was found that age, time to hospitalization, blood paraquat level, estimated glomerular filtration rate at admission (eGFR first day), and the SOFA48-h score, but not the AKIN48-h score, were significant predictors of mortality. For predicting the in-hospital mortality, SOFA48-h scores displayed a good area under the receiver operating characteristic curve (AUROC) (0.795±0.033, P<0.001). The cumulative survival rate differed significantly between patients with SOFA48-h scores <3 and those ≥3 (P<0.001). A modified SOFA (mSOFA) score was further developed by using the blood paraquat level, and this new score also demonstrated a better AUROC (0.848±0.029, P<0.001) than the original SOFA score. Finally, the cumulative survival rate also differed significantly between patients with mSOFA scores <4 and ≥4 (P<0.001).ConclusionThe analytical data demonstrate that SOFA and mSOFA scores, which are based on the extent of organ function or rate of organ failure, help to predict mortality after intentional paraquat poisoning.

A substantial proportion of paraquat patients suffered from hepatic complication (46.52%), but the spectrum of hepatitis in these patients seemed mild and transient.

Studies indicate that environmental exposure to lead is associated with reduced renal function. Whether lead affects progressive diabetic nephropathy is unclear. Eighty-seven patients with type II diabetes and diabetic nephropathy (serum creatinine of 1.5-3.9 mg/dl) with normal body lead burden and no lead exposure history were observed over a 12-month period. Thirty subjects with high normal body lead burdens (80-600 microg) were randomly assigned to a chelation and control group. For 3 months, the 15 chelation-group patients underwent lead-chelation therapy with calcium disodium ethylenediaminetetraacetic acid weekly until body lead burden fell <60 microg, and the 15 control group subjects received a weekly placebo. During the following 12 months, renal function was regularly assessed at 3-month intervals. The primary outcome was an elevation of serum creatinine to 1.5 times baseline value during the observation period. A secondary outcome was temporal changes in renal function following chelation therapy. Twenty-six patients achieved the primary outcome. Basal blood lead levels and body lead burden were the most important risk factors in predicting progressive diabetic nephropathy. Following chelation, the rates of decline in glomerular filtration rates in the chelation group and the control group, respectively, were 5.0+/-5.7 ml and 11.8+/-7.0 ml/min/year/1.73 m(2) of body surface area (P=0.0084) during follow-up, although both groups had similar rates of progression of renal function during the 12-month observation period. We concluded that low-level environmental lead exposure accelerates progressive diabetic nephropathy and lead-chelation therapy can decrease its rate of progression.

In May 2011, the illegal use of the phthalate plasticizer di(2-ethylhexyl) phthalate in clouding agents for use in foods and beverages was reported in Taiwan. This food scandal has caused shock and panic among the majority of Taiwanese people and has attracted international attention. Phthalate exposure is assessed by ambient monitoring or human biomonitoring. Ambient monitoring relies on measuring chemicals in environmental media, foodstuff and consumer products. Human biomonitoring determines body burden by measuring the chemicals, their metabolites or specific reaction products in human specimens. In mammalian development, the fetus is set to develop into a female. Because the female phenotype is the default, impairment of testosterone production or action before the late phase may lead to feminizing characteristics. Phthalates disrupt the development of androgen-dependent structures by inhibiting fetal testicular testosterone biosynthesis. The spectrum of effects obtained following perinatal exposure of male rats to phthalates has remarkable similarities with the human testicular dysgenesis syndrome. Epidemiological studies have suggested associations between phthalate exposure and shorter gestational age, shorter anogenital distance, shorter penis, incomplete testicular descent, sex hormone alteration, precocious puberty, pubertal gynecomastia, premature thelarche, rhinitis, eczema, asthma, low birth weight, attention deficit hyperactivity disorder, low intelligence quotient, thyroid hormone alteration, and hypospadias in infants and children. Furthermore, many studies have suggested associations between phthalate exposure and increased sperm DNA damage, decreased proportion of sperm with normal morphology, decreased sperm concentration, decreased sperm morphology, sex hormone alteration, decreased pulmonary function, endometriosis, uterine leiomyomas, breast cancer, obesity, hyperprolactinemia, and thyroid hormone alteration in adults. Finally, the number of phthalate-related scientific publications from Taiwan has increased greatly over the past 5 years, which may reflect the health effects from the illegal addition of phthalate plasticizer to clouding agent in foodstuff over the past two decades.