Lead in a case of encephalopathy.

A 2-year-old boy with a history of pica was admitted with vomiting and treated overnight for viral tonsillitis. A week later, he presented with a prolonged afebrile seizure and required intubation and ventilation. Antibiotics and acyclovir were started. Despite extensive investigations including MRI head, no cause was identified. Four days later, he deteriorated with signs of raised intracranial pressure. On day 5, blood lead concentration in the sample collected at admission was reported as grossly elevated, consistent with a diagnosis of severe lead poisoning from ingesting lead-containing paint at the family home. Chelation therapy was started but, unfortunately, he did not make a neurological recovery, and care was withdrawn. A serious case review identified a lack of awareness of lead poisoning and its relation to pica as a root cause. We report this case to share our experience and the importance of considering lead poisoning in children with pica.

Methemoglobinemia in a Case of Paint Thinner Intoxication, Treated Successfully with Vitamin C.

BACKGROUND: Methemoglobin (MetHb) is an oxidized form of hemoglobin. It is a poor transporter of oxygen and is unable to deliver oxygen to the tissue. Globally, drug & toxin induced methemoglobinemia is more common as compared with the congenital form. Methemoglobinemia caused by paint thinner intoxication is rare. Methylene blue is well established as the first-line therapy for severe methemoglobinemia. CASE REPORT: A 25-year old man was brought to the Emergency Department after accidental consumption of paint thinner. On clinical examination, he had cyanosis and there were discrepancies in his pulse oximetry and arterial blood gas (ABG) analysis results. With this clue and supporting laboratory investigations, the diagnosis of toxin-induced methemoglobinemia was made. Due to the unavailability of methylene blue, alternative treatment with high-dose vitamin C was attempted, to which the patient responded. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: The role of vitamin C in the treatment of methemoglobinemia has not been well established, with only a few published case reports. This patient had severe methemoglobinemia, with MetHb of 46.4%, which responded dramatically to vitamin C therapy, with no side effects. This case shows that high-dose vitamin C is safe and has the potential to be an effective alternative for the treatment of severe methemoglobinemia. In the presence of cyanosis, mismatch of pulse-oximetry and ABG-analysis are the key for the physician to suspect methemoglobinemia.

Child and maternal household chemical exposure and the risk of acute leukemia in children with Down's syndrome: a report from the Children's Oncology Group.

Compared with the general pediatric population, children with Down's syndrome have a much higher risk of acute leukemia. This case-control study was designed to explore potential risk factors for acute lymphoblastic leukemia and acute myeloid leukemia in children with Down's syndrome living in the United States or Canada. Mothers of 158 children with Down's syndrome and acute leukemia (97 acute lymphoblastic leukemia, 61 acute myeloid leukemia) diagnosed between January 1997 and October 2002 and mothers of 173 children with Down's syndrome but without leukemia were interviewed by telephone. Positive associations were found between acute lymphoblastic leukemia and maternal exposure to professional pest exterminations (odds ratio = 2.25, 95% confidence interval: 1.13, 4.49), to any pesticide (odds ratio = 2.18, 95% confidence interval: 1.08, 4.39), and to any chemical (odds ratio = 2.72, 95% confidence interval: 1.17, 6.35). Most of the associations with acute myeloid leukemia were nonsignificant, and odds ratios were generally near or below 1.0. This exploratory study suggests that household chemical exposure may play a role in the development of acute lymphoblastic leukemia in children with Down's syndrome.

Air pollution and atopy.

Relationships between air pollutants and atopy can be studied within 3 different settings. In vitro, exposure of pollen to air pollutants induce morphological changes and seems to facilitate extrusion on allergenic material out of the pollen grain. In animal as well as in human experiments, air pollutants, especially diesel exhaust particulates, are able to trigger an IgE-response. Epidemiological surveys also show that air pollutants trigger symptoms in patients. In contrast, whether or not air pollutants can induce de novo allergic diseases is still a matter of debate. Some surveys suggest that, in humans also, air pollutants, especially diesel-exhaust particulates, could trigger allergic sensitization and development of atopic diseases. At home, other pollutants can be involved: volatile organic compounds have pro-inflammatory properties and favour T-cell sensitization. Relationship between exposure to secondhand tobacco smoke or occupational hazards and atopic sensitization have led to discordant results.

Patch test results in 542 patients with suspected contact dermatitis in Turkey.

In this retrospective study, patch test results of 542 patients (303 female and 239 male), referred to our clinic between June 1996 and July 1999, were evaluated. All patients were patch tested with 32 allergens of an extended European standard series, 140 patients were tested with supplemental series, and 246 patients with their own substances. 280 (51.7%) patients had 1 or more positive results but allergic contact dermatitis, according to clinical relevance, was diagnosed in only 190 (67.9%) of these. Nickel sulfate was the most frequent sensitizer (19.1%), followed by potassium dichromate (11.8%), palladium chloride (9.4%), cobalt chloride (8.5%), and thiuram mix (7.7%). Frequencies of contact allergy to fragrance mix (5.5%), balsam of Peru (Myroxylon Pereirae resin) (2%), quaternium-15 (0.6%), and Kathon CG (methylchloroisothiazolinone+methylisothiazolinone) (0.2%) were relatively low, while no positive reactions were obtained to paraben mix in any case. Current clinical relevance to the present dermatitis was most frequently seen with carba mix (96.2%), thiuram mix (95.2%) and potassium dichromate (78.1%), whereas this rate was low for nickel (37.5%). In 85.8% of patients with allergic contact dermatitis, the responsible allergen was detected by testing with the extended standard series alone (18.4% identified by testing with the additional 10 allergens), in 11.6% by testing with the patients' own substances, and in 2.6% by testing with the supplemental series. Occupational contact dermatitis was diagnosed in 77 of the patients with positive reactions (27.5%), most of these being construction workers and house painters who showed relevant sensitizations to potassium dichromate, cobalt chloride, thiuram mix and carba mix. There was no statistically significant difference in the total contact sensitization rate between atopics and non-atopics, but contact sensitivity to nickel sulfate and palladium chloride was significantly higher among atopics. MOAHL index in % was: 44.1/14.2/24.9/ 54.4/2.4. In conclusion, we believe that similar large series of patients would be helpful to delineate the exact profile of contact dermatitis in Turkey.

Time required for blood lead levels to decline in nonchelated children.

OBJECTIVE: To determine the time for a decline in blood lead to less than 10 microg/dL in nonchelated children who are enrolled in case management. STUDY DESIGN: Retrospective analysis of venous blood lead data of lead-poisoned children followed in a case management program designed to decrease lead exposure. Children were excluded if their blood lead had not yet declined to less than 10 microg/dL, if they received chelation therapy, or if they had not received follow-up for more than 15 months. We calculated the time between peak elevation of lead and decline to less than 10 microg/dL. Data were categorized based on the child's peak blood lead and season in which their peak blood lead occurred. Data were analyzed using ANOVA and linear regression. Kaplan-Meier survival analysis was used to describe data in population form. RESULTS: 579 patients were included in the analysis. Blood leads of 25-29, 20-24, 15-19, and 10-14 microg/dL required 24.0, 20.9, 14.3, and 9.2 months, respectively, to decline to less than 10 microg/dL. For continuous data, a linear relationship was described by the following equation: Time (# of months required to achieve a blood lead less than 10 microg/dL) = 0.845 x peak lead; p < 0.0001. Kaplan-Meier curves complement the findings in a population-based fashion. CONCLUSIONS: The mean time for blood lead to decline was linearly related to the peak in blood lead. The time for 50% of the blood lead to decline to less than 10 microg/dL was not linear and varied with peak lead.

[Intake of heavy metals (lead, cadmium, zinc) originating from colored paints and their incorporation into organs and tissues of heifers]. / Untersuchungen zur Aufnahme von Schwermetallen (Blei, Cadmium, Zink) aus Farbanstrichen und deren Einlagerung in Organe und Gewebe von Jungrindern.

In a feeding trial the effect of heavy metals as lead, cadmium and zinc originating from colour paints was investigated. The study included 30 early pregnant heifers subdivided in five groups with six animals each with an average body weight of 419 kgs. During the testing period the trial was carried out in a three factorial fashion with two time sections: section one--mineral supplementation and lead preexposure; section two--Exposure to heavy metal containing colour paint pigments. The investigation led to the following results: A short time uptake of daily 10 g lead containing colour paint (i.e. 22-24 mg Pb/per animal and day) did not cause any change of general health and normal behavior of the respective animals. A storage of lead in the body tissue could be observed by way of a hint. An additional prestress with lead (145-158 mg Pb/animal/day over a period of 84 days did not influence the general health of the animals significantly. Both the fodder uptake and the body weight gain was inconspecious. A storage of lead could be traced in the skeleton, kidney and liver and--on a reduced level--also in the muscle. Only the content of lead in the kidney exceeded the maxmium tolerated value (> 1.0 mg/kg) of the German Meat Hygiene regulation. A mineral deficient feeding regimen (especially lack of calcium) enhance an increased storage of lead in the tissues (skeleton).

Moderate lead poisoning: trends in blood lead levels in unchelated children.

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.

Occupational exposure to hydrocarbons and chronic pancreatitis: a case-referent study.

OBJECTIVES: To investigate the hypothesis that hydrocarbon exposure is a risk factor for chronic pancreatitis. METHODS: 102 cases of chronic pancreatitis and 204 age and sex matched referents were interviewed about their occupational histories, alcohol and cigarette consumption, and diet. Exposure to hydrocarbons was inferred from interview responses by four assessors who were blind to disease state, and these data were then summarised by a cumulative hydrocarbon exposure (CHE) score. RESULTS: After adjustment for alcohol, cigarettes, dietary antioxidants, and social class, odds ratios for low CHE scores were 1.20 (90% CI: 0.62-2.35) and 2.67 (90% CI: 1.22-5.87) for high scores. A test for trend with level of exposure among only those who had exposure scores > 0 gave p = 0.09. Analysis by type of hydrocarbon was limited to four exposures for each of which there were at least 20 exposed patients. The adjusted OR for paint solvents (any level) was 0.96 (90% CI: 0.48-1.93); for diesel exhaust fumes OR = 2.66 (90% CI: 1.05-6.73); for petrochemicals OR = 1.82 (90% CI: 0.80-4.11); and for chlorinated solvents OR = 1.49 (90% CI: 0.58-3.81). CONCLUSIONS: These results support the original hypothesis. Further studies are needed to confirm or refute the findings here and to clarify the types of hydrocarbon involved.

Residential deleading: effects on the blood lead levels of lead-poisoned children.

Acute elevations of venous blood lead levels (PbB) are periodically reported in children with chronic lead poisoning, during deleading of their houses. To evaluate this phenomenon 114 preschool children who entered the Massachusetts Childhood Lead Poisoning Prevention Program case management system during 1984 and 1985 were retrospectively studied. PbB increased from a mean (+/- SE) of 1.76 +/- 0.03 mumol/L (36.4 +/- 0.6 micrograms/dL) prior to deleading to 2.03 +/- 0.07 mumol/L (42.1 +/- 1.5 micrograms/dL) during deleading (P less than .001). Among 41 subjects for whom deleading was done by dry scraping and sanding, the mean mid-deleading PbB was higher than the pre-deleading PbB by 0.44 +/- 0.12 mumol/L (9.1 +/- 2.4 micrograms/dL). However, when deleading was done by covering or replacement of painted surfaces in the residences of 12 subjects, mid-deleading PbB decreased 0.11 +/- 0.12 mumol/L (2.25 +/- 2.4 micrograms/dL) (P less than .005). In a subset of 59 subjects who had no chelation therapy and were available for follow-up 250 +/- 14 days after completion of deleading, PbB had decreased from 1.72 +/- 0.04 mumol/L (35.7 +/- 0.9 micrograms/dL) to 1.24 +/- 0.04 mumol/L (25.5 +/- 0.9 micrograms/dL) (P less than .001). The long-term effect of deleading is a significant reduction in PbB. However, deleading resulted in a significant, albeit transient, increase in PbB.

Demographic data and treatment of small companion animals with lead poisoning: 347 cases (1977-1986).

Three hundred forty-seven cases of lead poisoning in small animals, diagnosed after 1976, were reviewed. The types of treatments used and their outcomes were analyzed. Changes in blood lead concentrations following various treatments, as well as the sources of lead exposure, were also reviewed. The geographic origins of the cases were traced, and demographic factors were studied to determine possible correlates that might explain the regional distribution of cases.

Lead poisoning in adults from renovation of an older home.

Presented is the case of a group exposure to lead occurring during the removal of lead-based paint from an older home. One patient had symptoms from the time of exposure to the time of presentation, when he was acutely ill and encephalopathic. The patient was treated successfully with an initial course of British Anti-Lewisite agent and calcium disodium versenate (CaEDTA) chelation, and two subsequent chelations with CaE-DTA alone. The other two patients had elevated lead levels but were asymptomatic. They were followed closely, and their lead levels steadily declined over several months. The evaluation and treatment of lead poisoning and excessive lead levels in adults is discussed, as is the need for physicians and the lay public to become aware of the hazards of renovating older homes.

Lead intoxication in Sydney Harbour Bridge workers.

Thirty-eight Sydney Harbour Bridge workers were assessed for possible lead intoxication. Forty-seven per cent were found to have significant lead intoxication as assessed by calcium disodium edetate chelation (Ca EDTA) testing and were subsequently effectively and safely treated with Ca EDTA. The prevalence of neurological, constitutional, gastrointestinal and musculoskeletal symptoms was significantly greater in those with, than those without, lead toxicity. Although blood lead levels and, to a lesser extent, hematological parameters were of some use in diagnosis, they were not sufficiently sensitive and thus should not be used in screening workers at risk of lead intoxication. Ca EDTA testing remains the diagnostic method of choice. Patients exposed to lead dust and fumes, in whom symptoms of lead intoxication are present, should undergo such testing and if a positive result is obtained, then EDTA chelation therapy should be instituted.

Hazards of 'deleading' homes of children with lead poisoning.

"Deleading" the homes of children with lead poisoning is a necessary step to terminate the child's exposure to lead. Lead poisoning as a result of lead exposure during the process of deleading has occurred in deleading workers but has not been well documented among children whose homes are deleaded. We treated four children with classes I through III lead poisoning (range of blood lead [Pb-B] level, 1.6 to 2.75 mumol/L [33 to 57 micrograms/dL]) who had significant elevation of their Pb-B levels (range, peak 4.34 to 6.27 mumol/L [90 to 130 micrograms/dL]) following deleading of their homes. The methods used for deleading included scraping, sanding, and burning of the paint. Symptoms included irritability (n = 3) and vomiting (n = 1). The elevation of the Pb-B levels was detected early, allowing prompt chelation therapy. Because exacerbation of lead poisoning may occur in children following deleading of their homes, safer approaches of deleading should be determined.

Lead intoxication in paint removal workers on the Sydney Harbour Bridge.

Lead intoxication is far more prevalent than is recognized by those persons who are exposed to lead fumes and dust in industry, as the early symptoms of intoxication are subtle and non-specific. The levels of lead in blood are a poor reflection of lead stores in the body and their potential toxicity, but are used frequently as the only test for screening of lead intoxication. Chelation of lead with calcium-EDTA is a more sensitive test to detect those persons who are at risk of toxicity. Industrial workers who are exposed regularly to lead must be screened on a periodic basis and a diagnosis of lead poisoning must be considered if substantial morbidity is to be avoided. We report six cases of men with significant lead intoxication who were employed on the Sydney Harbour Bridge, all of whom have benefited symptomatically from calcium-EDTA chelation therapy.

Occupational factors and pancreatic cancer.

The relation between occupational factors and pancreatic cancer has been studied by two different approaches: a population based case-control study with two series of controls and a retrospective cohort study based on register data. With both approaches, some support was found for an association with occupational exposure to petroleum products. Associations were also indicated with exposure to paint thinner (case-control study) and work in painting and in paint and varnish factories (cohort study), for exposure to detergents, floor cleaning agents, or polish (case-control study) and with floor polishing or window cleaning (cohort study), and for exposure to refuse (case-control study) and work in refuse disposal plants (cohort study).

Solvent containing processes and work practices: environmental observations.

Even though there has been a shift toward water-based or fully solid systems, organic solvents still comprise a significant occupational health hazard. Fortunately, exposure levels can nowadays be effectively controlled by proper enclosures and ventilation in most remaining applications of organic solvents, and, generally taken, the development of occupational health conditions has been favorable on the workplaces using organic solvents. When as many as 24.2% of the 2639 solvent measurements carried out by the Institute of Occupational Health in Finland exceeded the occupational health standards between 1971 and 1976, such non-compliance levels were detected only in 3.0% of the 2823 samples taken between 1977 and 1980 (Skyttä, 1978; Kokko, 1982). The persons dealing with occupational health problems in workplaces should also be aware of the possible existence of solvent misuse. This may not develop into the level of solvent sniffing, but into a milder addiction. The workers adopt working habits that cause unnecessary exposure. Repeatedly found exceptionally high concentration levels in biological exposure tests are an indication of a possible abuse.

The relationship between the level of lead absorption in children and the age, type, and condition of housing.

A group of 184 preschool-aged children with pretreatment blood lead concentrations (PbB) greater than or equal to 50 micrograms/dl, who received inpatient chelation therapy, were followed prospectively as outpatients for 12 months after discharge. Of these, 160 were followed for 24-30 months. Serial PbB data were analyzed according to the type of housing to which each child was discharged. Following therapy, PbB stabilized by 3 months. Thereafter, highly significant differences (P less than 0.001) existed between those living in or visiting old houses in which lead-in-paint hazards had been abated according to local ordinances (m PbB = 38.5 micrograms/dl) and those discharged to "lead-free" public housing (m PbB = 28.8 micrograms/dl) or to recently, totally gutted and renovated old housing (m PbB = 28.7 micrograms/dl). During the period of study (1978-1982), no downward trend in PbB within housing groups was found during the first 12 months of follow-up. Of the 152 children discharged to old housing, 75 had 127 recurrences of PbB greater than or equal to 50 micrograms/dl. This emphasizes the need for close and prolonged follow-up in all cases. These data indicate that substantially improved methods of detection, classification, and abatement of lead hazards must replace traditional methods if lead exposure for young children in old housing is to be reduced to an acceptable level.