Background: Lead poisoning has proven to be one of the most important environmental health problems among developing countries with both direct and indirect effects on human life. Lead is known to cross the blood-brain barrier and placenta, and accumulates in soft and hard tissues. Lead can be excreted in urine, stool, milk, sweat, nails and saliva. During pregnancy and lactation, lead is released from bones into the blood along with Ca2+. The toxic effects of lead on various human tissues have been studied extensively, but few studies have addressed its impact on fetal development during pregnancy. Blood levels of lead are higher in people living in lead-polluted regions. It has been reported that Tehran (central and southern parts) is the most problematic city in terms of lead poisoning.
Methods: From 86 sets of mothers and newborns in a non-polluted area of rural Rasht, Iran, we examined specimens of maternal blood, cord blood and colostrum (86×3=258) and specimens from 85 sets of mothers and newborns in a polluted area of Tehran, Iran (85×3=255) for lead levels using atomic absorption spectrophotometry (AAS) and analyzed the results by t-test, SPSS, and linear regression.
Results: The mean blood lead concentrations of mothers, cord blood of newborns and colostrum were 7.6±4.1, 5.9±3 and 4.2±2.5 μg/dl, respectively, in the non-polluted area and 9.1±8.4, 6.5±5.2 and 5.8±5.5 μg/dl, respectively, in the polluted area. The mean weights of the newborns in non-polluted and polluted areas were 3.2±0.5 kg and 3.2±4.5 kg, respectively.
Conclusions: Our data revealed an association between mean concentrations in blood lead of mothers and newborns and between mean concentrations of colostrum lead and newborn blood lead in both areas (p=0.01). There was no association between mean blood lead concentration of mothers with the weight of their newborns (p=0.89).
Background: Exposure to low levels of lead increases blood pressure in humans and animals. Although there are controversial reports about the exact mechanisms of lead-induced hypertension, many factors such as alteration in the cardiovascular responsiveness to endogenous substances including catecholamines could be one of the mechanisms involved. In the present study, the effect of lead acetate on the systolic blood pressure and responsiveness to β-adrenergics was investigated in rats.
Methods: Through their drinking water, three groups of rats were exposed to 100 ppm lead acetate for periods of 4, 8 or 12 weeks. The blood pressures of the rats were monitored throughout the study. The rat hearts were isolated and perfused with Krebs-Henseleit solution (pH=7.4) at 37˚C and gassed with 95% O2 + 5% CO2. The heart rate (chronotropic) and contractile (inotropic) responses were recorded before and after adding isoproterenol at multiple concentrations to the perfusion solution.
Results: The mean blood pressures in the 8 and 12-week lead-treated groups were significantly higher than that of the control group (P<0.01). The chronotropic response to many doses of isoproterenol was significantly increased in the 12-week lead-treated group compared to that of the control group (P<0.05). The inotropic response to this drug was significantly increased in both the 8- and 12-week lead-treated rats (P<0.05 and P<0.01, respectively).
Conclusions: Our results indicate that low-levels of lead increase systolic blood pressure as well as both chronotropic and inotropic effects of β-adrenergics, which could imply an important role in the pathogenesis of lead-induced hypertension.
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Background: Lead poisoning could be associated with
gastrointestinal renal, hematologic complications and neurologic deficit.
Case report: The patient was an opium addict, forty
one years old male, to hospital admitted with gastrointestinal signs,
constipation, abdominal pain, severe weakness of upper and lower limbs without
any sensory impairment and with anemia, leukocytosis, and slightly increased
liver function tests. Serum level of lead was more than 200µg/dl.
After treatment with dimercaprol (BAL),
CaNa2EDTA
for two five days sessions that followed with oral succimer for three days,
signs and symptoms relieved, all laboratory tests became normal and blood level
of lead reduced but the patient was discharged with quadriplegia. There was no
fecal or urinary incontinence.
Conclusions: Because of irreversibility and severity of lead related neuronal injury,
we should suspect to lead poisoning in each patient with neuronal involvement
and concurrent GI and hematologic signs.
Background: Convulsion is one of the common cause of hospital admission in children. Idiopathic seizure is when no anatomic, electrolytic, metabolic or hemorrhagic causes are found. Recently, lead poisoning, which is considered when serum lead levels are higher than the normal levels (previously 10 &mug/dl changed to 5 &mug/dl). Even lower levels of lead inflict harmful consequences in central nervous system (CNS) development in pediatric group. Due to air pollution and high lead level in air of Tehran, investigation the probable role of lead in producing or predisposing convulsion in children is very important. To determine the cerebrospinal fluid (CSF) lead level in children with idiopathic convulsion in compare with nonconvulsive ones (control). Methods: A case-control study upon 60 children (30 convulsive and 30 nonconvulsive control) admitted in Rasoul Akram and Ali Asghar University Hospitals, Tehran, from 2012 to 2013 had done. One ml of CSF obtained and lead level determined by atomic absorption test. Results: The mean age between cases and controls was not different (mean= 30.18+27.36 vs 25.46±20.56 months, P= 0.1). The CSF lead level (&mug/dl) had not meaningful difference between 2 groups (3.43+3.07 vs 2.78+2.77, P= 0.3), and no related to type of convulsion in cases (P= 0.7), the area under the curve (AUC) was 0.588 1-0.433, P= 0.2). The CSF lead cutoff was 1.65 &mug/dl sensitivity of 70%, specificity of 46%, PPV and NPV was 56% and 60% respectively. Conclusion: The toxic blood level for lead is 3.5 &mug/dl. The CSF lead level even in little amount (1.65 &mug/dl) is an acceptable sensitivity but lower specificity for differentiation the convulsive from nonconvulsive children. Although the role of genetic and other causes should be considered in idiopathic convulsion, probably, the high level of lead in CSF could predispose those children to convulsion. It can effect CNS development in children even in small amounts. Indeed, long-term effects of lead which continue to adulthood should be considered as well. Hence, it is paramount to rectify the ambient air lead pollution in Tehran.
Conclusion: Lead poisoning could potentially damage liver function and elevate liver enzymes. Moreover, it can also affect the levels of TSH and levothyroxine. Understanding the exact mechanisms might help to control The hepatotoxic effects of lead in patients. Also, knowing the pattern of elevated liver enzymes and thyroid hormones changes might help discriminate lead poisoning with other differential diagnoses.
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