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Among the heavy metals, lead still remains the major toxic pollutant of the environment. Human exposure to lead can occur through numerous pathways including air, food, dust, soil, and water. In the present study 14 lead poisoned patients with non-occupational lead exposure were evaluated. They were followed up and compared against the controls with no history of lead exposure. The patients had high blood lead levels and symptoms of weakness, dizziness, abdominal pain, generalized body ache, loss of appetite, and anxiety. Repeated course of chelation therapy helped to bring down their body burden of lead. Alternative sources for lead exposure can cause severe lead poisoning in general population. Screening and medical management of such individuals is very important to identify and eliminate sources of lead. The treatment and management requires a thorough medical evaluation and environmental intervention.

We report a case of acute lead poisoning in an adult female who had last been exposed to lead 7 years ago. She presented with abdominal pain, knee pain, and neurological symptoms, hypertension, chronic kidney disease, and anemia with basophilic stippling and lead gum lines. Compared to during her recent pregnancy, her lead level had almost tripled in 5 months to 81 mcg/dL. Chelation therapy was initiated and improved the patient’s symptoms and lead level significantly. In the absence of any new lead exposure or other reasons for increased bone turnover, this acute lead increase was likely due to skeletal mobilization caused by increased resorption from mineralized tissue during and after her pregnancy. This case report illustrates the seriousness of long-term health effects associated with lead poisoning at a multi-organ level, even years after the initial exposure. Thus, patient care should not be limited to the acute treatment of increased lead levels, but also include prevention of increased mobilization and bone turnover and appropriate patient education. In this context, we review various aspects of lead toxicity, especially during pregnancy and lactation.

Although the majority of published cases of lead poisoning come from occupational exposures, some traditional remedies may also contain toxic amounts of lead. Ayurveda is a system of traditional medicine that is native to India and is used in many parts of world as an alternative to standard treatment regimens. Here, we report the case of a 58-year-old woman who presented with abdominal pain, anemia, liver function abnormalities, and an elevated blood lead level. The patient was found to have been taking the Ayurvedic medicine Jambrulin prior to presentation. Chemical analysis of the medication showed high levels of lead. Following treatment with an oral chelating agent, the patient's symptoms resolved and laboratory abnormalities normalized. This case highlights the need for increased awareness that some Ayurvedic medicines may contain potentially harmful levels of heavy metals and people who use them are at risk of developing associated toxicities.

The appropriate clinical management of children who are moderately poisoned with lead (Pb) is under active investigation. To determine the pattern of change in blood Pb (BPb) levels in the absence of chelation therapy, we followed moderately Pb-poisoned children (initial blood Pb levels 1.21-2.66 mumol/l or 25-55 micrograms/dl) for 6 months with repeated BPb level measurements. Chelation therapy was not administered because all the children had negative lead mobilization tests indicating limited response to the chelating agent, calcium disodium edetate (CaNa2EDTA). Eligible children received the following interventions: notification of the health department to remediate lead hazards; reinforced educational efforts about the toxicity sources and treatment of Pb during 10 clinic and 3 home visits; and iron therapy for children with ferritin levels less than 16 micrograms/l. To quantify the lead paint hazards in the home, we combined a visual rating of the surfaces (intact to peeling) with an X-ray fluorescence (XRF) measurement of the lead content of the painted surface. The sum of these assessments is termed the home environmental score (HES). Data were analyzed from 79 children. BPb levels declined by 27%, on average, over 6 months. HES was correlated with BPb at enrollment, but neither the initial nor later HES measurements predicted BPb at other time points. The HES was highest at enrollment and declined by 50% and 75% at the second and third home visits, respectively. However, only a minority of the children (20%) achieved an HES of 0, indicating no lead paint hazards at home. Despite some ongoing Pb exposure, a parallel fall in BPb levels was observed in subgroups of children with either initially low or high HES (above or below the median HES of 37). Iron status did not account for the change in BPb levels. These data provide evidence that our measure, the HES, is quantifiably related to BPb levels in children, that this correlation is significant only prior to intervention; and that BPb levels decline in children who are moderately poisoned with Pb after they are enrolled in a comprehensive intervention program, even in the absence of chelation therapy and in the presence of ongoing lead paint exposure and Fe deficiency.

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Saito, K. (1973).British Journal of Industrial Medicine,30, 352-358. Electroencephalographic studies on petrol intoxication: comparison between nonleaded and leaded white petrol. The effect of nonleaded and leaded petrol on the brains of rats was studied electroencephalographically. Bipolar electrodes were implanted on the brain surface between the frontal and occipital lobes of the left hemisphere. The rats were divided into two groups and were given by intraperitoneal injection 1 ml of either nonleaded white petrol (WP) or leaded petrol (LP) containing 1 000 ppm of tetraethyl lead per 100 g body weight. The electrocorticogram was observed for 10 days and the lead content of the brain, liver, and kidney was estimated.

The rats injected with leaded petrol showed excessive tension and excitement by the sixth or seventh day, and their body weight had diminished significantly by 10 days. One to three days after both LP and WP injection, the δ, θ, and α waves decreased significantly but the electrocorticogram from six or seven days after LP injection showed marked α and θ waves. The lead content in organs of the LP group was far greater than in those of the WP group and a correlation between the electrocorticogram and lead content was recognized.

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Childhood lead poisoning is characteristically a disease that occurs between the second and third years of life, generally resulting from the child's ingestion of lead-based paint or dust. However, lead poisoning may also appear in the first year of life. The case of a 4-month-old infant is reported in which the preparation of infant formula in a lead-soldered samovar (urn) resulted in venous blood lead levels as high as 46 microg/dl. The samovar had been brought into the United States by the parents while on a visit to Iran. The infant was placed on chelation therapy with parenteral CaNa2EDTA followed by oral meso-2,3-dimercaptosuccinic acid (DMSA) and d-penicillamine. This resulted in a rapid and substantial reduction in the blood lead level. Lead poisoning in infancy may have unusual etiologies such as in utero transmission of lead by lead-poisoned women. Because sources of lead poisoning in infancy may be unusual, a detailed environmental investigation may be necessary to identify the exact source. Children exposed to lead in the first 2 years of life have a special vulnerability to the neurotoxicity of lead, with the risk of enduring developmental handicaps. Continued public health initiatives to remove lead from the environment, in conjunction with routine lead screening of young children, will be key in meeting the goal of the Centers for Disease Control and Prevention to eliminate childhood lead poisoning by the year 2011.

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Traditional laboratory tests for lead poisoning tend to fail in cases where a considerable interval has elapsed since exposure. We have used calcium ethylene-diamine-tetra-acetate (CaNa2EDTA) for the quantitative mobilization of lead for diagnostic purposes.

In a control group of 50 individuals who had never worked with lead it was found that the average urinary excretion of lead in 24 hours amounted to 0·031 to 0·043 mg. The maximum value did not exceed 0·100 mg. After intravenous injection of CaNa2EDTA the amount of excreted lead rose considerably, but did not exceed 0·350 mg./24 hr.

In a group of 47 individuals who had formerly worked with lead or who were still engaged in this work but did not show any symptoms of poisoning, the urinary lead levels before injection were higher than in the control group. After injection of CaNa2EDTA the lead excretion in 24 hours increased considerably. After injection of CaNa2EDTA, patients suffering from chronic lead poisoning showed a considerable increase of urinary lead excretion, which attained the order of milligrams in 24 hours.

The fractionated examination of the urine of 10 unexposed individuals, undertaken at intervals of three hours, showed after injection of CaNa2EDTA no higher lead concentration than 0·500 mg./litre, the highest concentrations being observed six hours after injection. In the urine of individuals exposed to lead or suffering from lead poisoning a higher urinary lead concentration was found than in the control group, and the maximum was in these cases found at various time intervals.

It is concluded that the mobilization of lead may be of considerable value in the diagnosis of atypical cases of chronic lead poisoning, but the results can be evaluated only in association with the general clinical picture.

Blood lead concentrations were measured in 62 Asian children, of whom 37 had definitely had surma applied to their eyes and 25 were thought not to have done. The mean concentration in those who had not used surma was 0.98 +/- SD 0.42 mumol/1 (20.3 +/- 8.7 microgram/100 ml) compared with 1.65 +/- 0.68 mumol/4 (34.2 +/- 14.1 microgram/100 ml) in those who had. Analysis of 29 different samples of surma showed 23 of them to be composed largely of lead sulphide. We conclude that the use of surma is associated with high blood lead concentrations. In our cases most of it had been obtained abroad, and hence government restrictions might be ineffective in limiting its use: a better method of prevention might be to inform the leaders of Asian communities of the risks.

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A series of 100 lead workers from different industries, 91 at work and nine admitted to hospital with lead poisoning, was studied in order to define more clearly the clinical and biochemical criteria of lead poisoning in three stages—(A) a presymptomatic state of lead exposure (37 men), (B) a state of mild symptoms or mild anaemia (45 men), and (C) frank lead poisoning with severe symptoms and signs (18 men).

The tests used were haemoglobin, reticulocyte count, and blood lead, and urinary lead, coproporphyrin, δ-aminolaevulinic acid (ALA), and porphobilinogen (PBG) estimations. Of these, the urinary lead was similar for all three groups and the blood lead estimation was of less value for determining the clinical group of the men than the haemoglobin and urinary coproporphyrin or ALA estimations, which correlated well with the clinical assessment and with each other but showed no correlation with the urinary and blood lead levels. PBG levels became raised only with the onset of symptoms of lead poisoning.

A haemoglobin of 13 g./100 ml. (90%) or less is a cautionary sign. Urinary coproporphyrin above 80 μg./100 mg. creatinine (800 μg./litre), ALA above 2·0 mg./100 mg. creatinine (2·0 mg.%), and PBG above 0·15 mg./100 mg. creatinine (0·15 mg.%) were almost always associated with symptoms or signs and were therefore considered to be the upper safety limits. Although the blood lead level does not differentiate between lead toxicity and lead exposure, values above 60 μg. lead/100 g. blood should alert the physician to carry out other tests.

In addition to the above tests, blood pressure, blood urea, and serum uric acid estimations were performed on all the men in order to elucidate the possible role of lead in the production of renal damage. Blood pressure and serum uric acid levels were similar for all three groups but the blood urea level was raised in group C. The reason for this finding was not established.

It was found that scrap metal burning, battery manufacturing, and ship-breaking constituted the gravest lead hazards encountered in this survey whereas wire manufacture constituted the least. Workers in the most modern factory, a car-body pressing plant, gave average values just below the danger levels for the urinary coproporphyrin and ALA estimations despite apparently efficient protective measures. This finding underlines the importance of the medical supervision of lead workers.

A clinical trial of oral calcium disodium versenate (E.D.T.A.) in eight lead workers is described. A short course of versenate given while the men continued at work produced no side-effects. Complete overhaul of the processes and protective devices was made in the factory.

Clinical, biochemical, and haematological improvement followed the removal of up to 250 mg. lead in each case.

The mode of action and possible uses and abuses of oral versenate are discussed.

A biphase program of screening and treating high-risk children for lead poisoning resulted in a 30% fall in mean lead values in the target areas over a 5-year period. The mean and median for subjects under 6 years was 4–10 μg/100 ml higher than for those over 6. Median for a high incidence area was 42 μg/100 ml in 1967 and 30.0 in 1971; for a low incidence area, 33 and 20 μg/100 ml in the equivalent years.

Ingestion of lead paint was observed or demonstrated by x-ray in 90% of 2200 patients treated in the Lead Clinic. Gross neurologic sequelae were limited to two cases of mild, persistent ataxia. Impaired intellectual performance was observed subsequently in several asymptomatic patients with initial blood lead levels (PbB) ≥ 100 μg/100 ml.

In Poland, children are exposed to lead from the combustion of leaded gasoline and industrial processes. Since the early 1990s, emission levels have declined, and a ban on leaded petrol is anticipated in 2005. Major industrial sources are located in Silesia Province and the copper mining centre (Legnica region). Concerns about, lead exposure in children date back to the 1980s; mean blood lead levels (BILL)reported in children living near lead smelters in Silesia exceeded 20ug/dl. in the 1990s, mean BLLs were decreasing, both in urban children and those living near lead industry. Lower than the CDC action level of 101ug/dl, they were however higher than mean values in children from the other countries, where leaded gasoline had already been banned. Childhood lead poisoning prevention requires a comprehensive approach, involving different sectors. Medical prevention focuses on the early detection of exposed child by the blood lead testing and individual case management. An increasing body of evidence, indicating adverse effects even below the current “safe” level of 101ug/dl, argues for intensification of the primary prevention, which requires legal, economic and technical measures. Public health efforts should contribute to the reduction and elimination of sources of exposure in child’s environment and public education campaigns.

Lead poisoning is well documented in persons occupationally exposed to lead. What is less known is, that even in persons working in lead based industries, the effect of lead and the appearance of signs and symptoms of lead poisoning is genetically determined. Three genes related to lead metabolism, exhibiting polymorphism have already been demonstrated-δALA-dehydratase, Vitamin D receptor gene and Hemochromatosis gene. These alleles determine the susceptibility of the individuals to lead. We present here a case of a lead acid battery worker, who presented without any signs and symptoms of lead poisoning except for a very high level of blood lead (82.8μg/dl and 47.5μg/dl 9 months later)

The effect of aqueous lead acetate given per os to chickens for 35 consecutive days and the effect of lead on interferon and antibody production was investigated. Chickens were found to tolerate levels of lead as high as 160 mg/kg/day without exhibiting clinical signs or hematological changes in spite of very high levels of lead in the blood (6.2 ppm). It is apparent from these findings that chickens are more resistant to lead poisoning than humans, horses, dogs and wild fowl such as ducks.

Subclinical lead doses did not affect interferon induction in response to statolon and Newcastle Disease virus (NDV)-B1. Interferon concentrations and duration in serum were markedly decreased in chickens which received lead at the 320 mg/kg level.

Long time lead exposure had no marked effect on antibody production to NDV in chickens. No consistent correlation was observed between blood lead concentration and antibody titer.

The results of these studies indicate that long term subclinical lead intake suppresses neither interferon nor antibody production in chickens.

Nine people from four families living in rural parts of Scotland have been found to suffer from clinical or biochemical effects of lead poisoning. Five had symptoms and four had unequivocal evidence of excessive lead exposure. The source of lead has been traced to the domestic water supply which in all cases was grossly contaminated with lead acquired from lead plumbing systems, including lead storage tanks. Clinical improvement followed the replacement of lead piping in two families studied. Lead poisoning is a possible cause of chronic ill health in areas of plumbosolvent water.

Background: In chronic petrol sniffers, recent exposure to high levels of leaded petrol may give rise to a lead encephalopathy characterised by tremor, chorea, ataxia, hyperreflexia, convulsive seizures, and death. Neurological abnormalities associated with lead encephalopathy involve the cortex, basal ganglia, cerebellum, and brain stem.

Objective: To use saccadic eye movement tasks as an experimental tool to determine which CNS changes are associated with chronic petrol sniffing and which with a history of lead encephalopathy, and to what extent these changes are reversible.

Methods: Saccade function was assessed in chronic petrol sniffers with a history of lead encephalopathy (encephalopathic sniffers), chronic petrol sniffers who had never suffered lead encephalopathy (chronic sniffers), individuals who had sniffed petrol in the past but had not done so for more than six months (ex-sniffers), and individuals who had never sniffed petrol (non-sniffers).

Results: Chronic sniffers showed increased latency of visually guided saccades and antisaccades and increased antisaccade errors which suggested cortical and basal ganglia dysfunction. These abnormalities returned to normal in ex-sniffers. Encephalopathic sniffers showed the same abnormalities as chronic sniffers but with greater severity and additional saccadic signs including dysmetria, gaze evoked nystagmus, and saccade slowing which usually indicate cerebellar and brain stem dysfunction.

Conclusions: Chronic petrol abuse is associated with cortical and basal ganglia abnormalities that are at least partially recoverable with abstinence. Additional long term cerebellar and brain stem abnormalities are associated with lead encephalopathy.

Chamberlain, M. J., and Massey, P. M. O. (1972).Brit. J. industr. Med.,29, 458-460. Mild lead poisoning with an excessively high blood lead. Lead poisoning occurred in a patient working as a smelter of precious metals on a process where lead was used as a substrate. Extremely high levels of blood lead up to 1 050 μg/100 ml were found despite only trivial clinical symptoms. Treatment consisted solely of removing the worker from the toxic environment. This resulted in complete recovery with return of the blood lead to a near normal value over the course of 12 months. Although there was only a mild anaemia present initially, the haemoglobin was slow to respond.

The Centers for Disease Control and Prevention recommend that local public health agencies use local data to identify children at risk for lead exposure to ensure that they receive preventive services. The objective of this study was to demonstrate the usefulness of a geographic information system (GIS) in identifying children at risk for lead exposure. We conducted a descriptive study, using GIS technology, of the blood lead (BPb) levels and residential location of at-risk children screened for lead exposure. "At-risk children" were defined as those children living in housing built before 1950 or in an area with a high proportion of older housing. The study was conducted in Jefferson County, Kentucky, USA. Participants were the cohort of children born in 1995 and screened from 1996 through 1997, and children younger than age 7 years who were screened from 1994 through 1998. Outcome measures were the BPb level and residential location (address or target zone) of at-risk children screened from 1996 through 1997, and the number and location of homes where more than one child had been poisoned by lead from 1994 through 1998. The proportion of children screened who live within zones targeted for universal screening varied from 48% to 53%, while only 50% of the at-risk children in the entire county were screened. Between 1994 and 1998, 79 homes housed 35% of the 524 children with lead poisoning. These housing units were prioritized for lead-hazard remediation. Significant numbers of at-risk children throughout the county were not being tested for lead exposure, even in prioritized areas. GIS can be very useful to health departments in planning lead exposure screening strategies and measuring program performance.

The three fatal cases of acute lead poisoning described show the difficulty experienced in reaching an early diagnosis of lead intoxication. A rapid micromethod is now available for the determination of whole blood lead levels on small samples of blood, using atomic absorption spectrophotometry.

Given an increased awareness of acute lead intoxication, the rapid confirmation of the diagnosis by the micromethod, and the early institution of adequate chelation therapy, then fatalities such as those described should not occur in the future.

Superwarfarin poisoning is considered a significant public health problem in the US. In 2004, there were 16 054 cases of poisoning; most were accidental ingestions of rat bait by children but 4576 patients required hospital treatment, 23 patients had major adverse outcomes and 1 patient died. Similar information is unavailable for the UK. The National Poisons Information Service is presently auditing cases.

The case of a farmer who presented with haematuria, 9 days after spilling a rodenticide containing a superwarfarin over himself is reported here. He was physically well except for mild abdominal tenderness. He had grossly deranged clotting studies (prothrombin time (PT) >200 s, activated partial thromboplastin time (APTT) 56 s) that were rapidly corrected with fresh frozen plasma and vitamin K. He was sent home after 5 days without follow up. Unfortunately, he presented again 2 days later, again with haematuria and an international normalised ratio (INR) >10. He required inpatient treatment with high‐dose vitamin K for 1 week. Upon discharge, he required daily vitamin K and INR monitoring for a further month. The original inpatient team had not identified the specific poison (chlorophacinone). They were unaware that superwarfarins are more potent and longer acting than warfarin, with toxic effects for weeks or even months, and that large doses of vitamin K are often required.

Studies in mice and guinea pigs have shown that albumin is a new biomarker of organophosphorus toxicant (OP) and nerve agent exposure. Our goal was to determine whether OP-labeled albumin could be detected in the blood of humans exposed to OP. Blood from four OP-exposed patients was prepared for mass spectrometry analysis by digesting 0.010 ml of serum with pepsin and purifying the labeled albumin peptide by offline high performance liquid chromatography. Dimethoxyphosphate-labeled tyrosine 411 was identified in albumin peptides VRY411TKKVPQVSTPTL and LVRY411TKKVPQVSTPTL from two patients who had attempted suicide with dichlorvos. The butyrylcholinesterase activity in these serum samples was inhibited 80%. A third patient whose serum BChE activity was inhibited 8% by accidental inhalation of dichlorvos had undetectable levels of adduct on albumin. A fourth patient whose BChE activity was inhibited 60% by exposure to chlorpyrifos had no detectable adduct on albumin. This is the first report to demonstrate the presence of OP-labeled albumin in human patients. It is concluded that tyrosine 411 of human albumin is covalently modified in the serum of humans poisoned by dichlorvos and that the modification is detectable by mass spectrometry. The special reactivity of tyrosine 411 with OP suggests that other proteins may also be modified on tyrosine. Identification of other OP-modified proteins may lead to an understanding of neurotoxic symptoms that appear long after the initial OP exposure.

To assess the risk of lead poisoning among preschool and school-aged children in Bangladesh, 345 children were screened for blood lead levels (BLLs) from one rural and two urban areas in Bangladesh from September 2007 through January 2008. An urban industrial area at Tongi was identified as a disaster area, where 99% (104/105) of those tested had BLLs ≥ 10 μg/dL. Industrial emissions and use of leaded gasoline by two-stroke engine vehicles were identified as possible sources of lead in that area. A rural nonindustrial area at Chirirbandar, Dinajpur was identified as another high-risk area, where 14% of the children screened had BLLs ≥ 10 μg/dL. BLLs at the urban industrial area were significantly higher than those at the rural and urban nonindustrial areas (24.58 ± 10.32, 7.24 ± 6.31, and 2.47 ± 3.32 μg/dL, respectively; p <0.001). Weight-for-age z-scores of the urban children were significantly lower than that of the rural children (–1.41 ± 1.88 vs. 0.20 ± 1.16, p <0.001). Children with elevated BLLs had poorer nutritional status (p = 0.05) than those with normal BLLs. Over 90% of the parents did not know that lead causes health problems. In conclusion, the problem of lead poisoning in children was found to be high in both urban and rural Bangladesh. A universal lead screening for preschool and school-aged children and a lead education program for parents are recommended for implementation in Bangladesh.

Amongst toxic heavy metals, lead ranks as one of the most serious environmental poisons all over the world. Exposure to lead in the home and the workplace results in health hazards to many adults and children causing economic damage, which is due to the lack of awareness of the ill effects of lead. We report the case of a 22 year old man working in an unorganized lead acid battery manufacturing unit, complaining about a longer history of general body ache, lethargy, fatigue, shoulder joint pain, shaking of hands and wrist drop. Patient had blue line at gingivodental junction. Central nervous system (CNS) examination showed having grade 0 power of extensors of right wrist & fingers. Reflexes: Supinator- absent, Triceps- weak and other deep tendon reflexes- normal. Investigations carried out during the admission showed hemoglobin levels of 8.3 g/dl and blood lead level of 128.3 μg/dl. The patient was subjected to chelation therapy, which was accompanied by aggressive environmental intervention and was advised not to return to the same environmental exposure situation. After repeated course of chelation therapy he has shown the signs of improvement and is on follow up presently.

Excessive lead exposure continues to be a pervasive and serious threat to the health and well-being of the nation's children. The current guidelines issued by the Centers for Disease Control and Prevention (CDC) recommend education (during well-child visits) regarding the major preventable sources of lead and how to prevent excessive exposure. To determine if parents receive counseling to prevent excessive lead exposure in their children, a survey of parental knowledge on prevention of lead exposure was administered to parents of children recently identified as having elevated blood lead levels. Surveys were administered by lead program outreach workers prior to an educational visit in urban neighborhoods of Boston, Massachusetts. Parents of 139 children (88% ethnic minorities; mean age: 31 months) with recently identified elevated blood lead levels (mean: 1 mumol/L) participated. Fifty-one percent first learned of their child's elevated lead level at the time they were contacted by an outreach worker. Seventy-one percent did not recall having been counseled regarding lead poisoning or its prevention prior to this contact. Before the outreach visit, 17% had been counseled but after the elevated lead was detected. Only 12% of the parents had received preventive counseling prior to detection of the elevated lead level. We conclude that despite CDC recommendations, adequate counseling for preventing lead poisoning does not occur for a substantial number of children who have elevated lead levels.

Seventy-four survivors of acute carbon monoxide poisoning were followed up for an average of three years. In eight patients gross neuropsychiatric damage was directly attributable to the poisoning. Three patients had committed suicide and eight had died from other causes. Morbidity and mortality in those deliberately and accidentally poisoned was approximately equal.

Of 63 patients alive at follow-up eight showed an improvement and 21 (33.3%) a deterioration of personality after poisoning, and 27 (43%) reported a subsequent impairment of memory. Deterioration of personality and memory impairment were highly correlated. The level of consciousness on admission to hospital in the acute phase of poisoning correlated significantly with the development of gross neuropsychiatric sequelae. These findings emphasize the importance of prompt and efficient treatment of carbon monoxide poisoning and the need to follow-up all cases in the anticipation of a relapsing course or the development of sequelae.