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Biomedical subjects

M A Majeed

Publications and source records attributed to M A Majeed.

At least 19 recordsLinked to original sources
PubMed2001

Methodologies for estimating emissions for the U.S. EPA's NOx SIP call, CER rule, and other complexities.

Emissions inventories play an important role in many air quality decisions, and the importance of obtaining correct emissions data challenges the emissions inventory community to continuously improve its estimation techniques. The Clean Air Act Amendments of 1990 requires states with ozone nonattainment areas (NAAs) to submit periodically a comprehensive, accurate, and actual inventory of ozone precursor emissions until the areas are redesignated to attainment. They require the states with NAAs to report peak ozone season daily and annual estimates of the inventories for the counties that are in nonattainment. The recently proposed U.S. Environmental Protection Agency's (EPA) NO(x) SIP call and the Consolidating Emissions Reporting (CER) rule are more demanding still. The CER rule requires the states to report statewide point source inventories, 3-yr cycle inventories, and NO(x) SIP call inventories by county for all source types, regardless of the attainment status; the estimating periods are peak ozone season daily, 5-month ozone season, and annual estimates. Furthermore, complexities in emissions inventories such as estimating the emissions with different seasonal and multiple controls exist. These complexities and methodologies for estimating emissions for different time periods are not addressed sufficiently either by the EPA's procedure manuals or by the Emissions Inventory Improvement Program guidance documents. This paper presents methodologies for estimating emissions for different time periods and multiple controls. These methodologies will help the EPA, state, and local government agencies to meet the evolving demands of emissions inventories and the reporting requirements of the NO(x) SIP call and the CER rules.

Air Pollutants↗
PubMed1981

Methylmercury poisoning in the Iraqi suckling infant: a longitudinal study over five years.

In a five-year longitudinal study of mothers and infants exposed to methylmercury during the Iraq epidemic of 1972, the frequencies of signs and symptoms exhibited by the mothers were typical of methylmercury poisoning. When blood concentrations of mercury are corrected to 1 March 1972, mothers with the most severe signs and symptoms had an average blood mercury concentration significantly higher (p less than 0.01) than either the milder or asymptomatic groups. Analytical data indicate that the predominant route of exposure for the infant was through breast milk in which approximately 60% of total mercury was determined, by cold vapor atomic absorption, to be organic mercury. Abnormal neurological signs in these infants became more obvious with time: hyperreflexia was observed in 8 of 22 infants at first examination, and in 17 of 22 at second examination. Delayed motor development became evident at the second and third examinations. The frequency of pathological reflexes and delayed motor developmental milestones was so high as to be considered significant even in the absence of a controlled study. There was no increase in mortality as compared to a control group.

Female↗
PubMed1981

Dose-response relationship for human fetal exposure to methylmercury.

Eighty-four Iraqi mothers and their infants had been exposed to methylmercury during pregnancy. The methylmercury had been ingested as a fungicide. Peak maternal hair mercury concentrations were related to the frequency of maternal symptoms during pregnancy and to neurological effects in the infants. These include various degrees of psychomotor retardation. Severe neurological deficits were observed in five children whose maternal peak hair mercury concentrations were 165 to 320 ppm. Minimal symptoms were reported for mothers and children when peak maternal hair levels were below 68 ppm. Minimal clinical neurological signs occurred in children when peak maternal hair mercury concentrations were at an undetermined point between 68 and 180 ppm. Greater fetal risk appears to be associated with exposure during the second trimester. This exposure to methylmercury was acute and the results may not be extrapolated to a constant level of exposure throughout pregnancy. The effects of fetal exposure to methylmercury in marine fish may differ.

Dose-Response Relationship, Drug↗
PubMed1981

Tests of efficacy of antidotes for removal of methylmercury in human poisoning during the Iraq outbreak.

Three complexing agents and a thiolated resin were tested for their ability to reduce the T 1/2 of methylmercury in blood during an outbreak of human poisoning. The slope of the line relating the natural logarithm of the blood concentration to time during treatment was calculated by a parametric (linear regression) and a nonparametric (two-point) method. The mean slope for each treatment group was calculated and the T 1/2 was calculated from the mean slope. Both the linear regression and two-point methods yield similar mean values. The "two-point" T 1/2 will be quoted here. The mean T 1/2 in six patients receiving no specific treatment was 65 days and in 10 patients receiving placebo was 61 days, and these values did not differ from those reported in the literature. All four treatments significantly reduced the mean T 1/2 values below the mean for the combined placebo and no treatment groups. Sodium 2,3-dimercaptopropane-1-sulfonate was the most effective agent, reducing the mean T 1/2 in 10 patients to 10 days. The thiolated resin given to eight patients produced a mean T 1/2 of 20 days. The penicillamines also produced a significant reduction in T 1/2 values; the mean T 1/2 for D-penicillamine in 12 patients was 26 days and N-acetyl-DL-penicillamine in 17 patients yielded a mean T 1/2 of 24 days. This is the first report of the effects of sodium 2,3-dimercaptopropane-1-sulfonate and resin in human subjects exposed to methylmercury. No adverse effects were observed in any of the treatment groups. A clinical trial was not possible but it is concluded that agents that reduce blood levels and accelerate excretion are probably clinically useful if given before irreversible damage has occurred.

Adolescent↗
PubMed1980

Fetal methylmercury poisoning: clinical and toxicological data on 29 cases.

This report describes psychomotor retardation in infants caused by prenatal exposure to methylmercury. A study of 29 mother-infant pairs established a relationship between maximum maternal hair mercury concentration during pregnancy and the frequency of neurological effects in the infants. The latter included delayed achievement of developmental milestones with or without neurological signs. The infants were 4 1/2 to 5 years of age on last examination. Ten infants of mothers who had maximum hair concentrations in the range of 99 to 384 pars per million (ppm) had a significantly higher frequency of abnormal findings than those in two groups having lower maternal hair mercury concentrations (12 to 85 and 0 to 11 ppm). The group sizes were too small to allow identification of a specific "threshold" maternal hair concentration above which such effects can be expected. Transient paresthesias during pregnancy occurred in 80% of the mothers in the higher concentration group (99 to 384 ppm) as compared with 30% and 22% in the lower groups. Neurological abnormalities were found in some children whose mothers had been asymptomatic during pregnancy.

Abnormalities, Drug-Induced↗
PubMed1980

Comparative study of the sensitivity of virgin and pregnant rats to methylmercury.

Pregnant and virgin female rats were dosed by gastric lavage 10 times or 5 times with 5 mg/kg mercury as methylmercury. Treatment of pregnant animals started on day 3 of gestation and ended on day 14 of gestation with two days break between the 5th and the 6th doses. In Group B, treatment lasted from day 10 to day 14 of gestation. Pregnant and virgin rats responded identically to methylmercury in terms of body weight changes, coordination disorders, and cerebellar histological changes. Furthermore, the brain, liver and kidney concentrations and the rates of methylmercury elimination in the post-treatment period were identical. Thus the results indicate no difference in sensitivity of pregnant versus non-pregnant animals.

Animals↗
PubMed1979

Prenatal methylmercury poisoning. Clinical observations over five years.

Thirty-two infants prenatally exposed to methylmercury and their mothers were examined over a five-year period after the Iraqi methylmercury epidemic. Severity of poisoning in mothers was related to the peak mercury concentration in their hair and in the infants to the maximum concentration in maternal hair during pregnancy. In nine cases of cerebral palsy, methylmercury exposure occurred only during the last trimester. All infants except three (two were orphaned soon after birth and one was bottle-fed) were exposed postnatally via suckling. Whereas the mother's symptoms usually improved, the damage to the fetal nervous system appears to be permanent. Milder cases previously not identified in other studies are reported. The syndrome consists of varying degrees of developmental retardation in addition to exaggerated tendon reflexes and the pathologic extensor plantar reflex (minimal brain damage syndrome).

Abnormalities, Drug-Induced↗
PubMed1978

Methylmercury poisoning in Iraqi children: clinical observations over two years.

The clinical features of 49 children who had eaten bread contaminated with methylmercury in rural Iraq were reviewed. Symptoms and signs relating to the nervous system--varying degrees of ataxia, weakness, and visual and sensory changes--dominated the clinical picture. The severity of poisoning was related to the blood mercury concentration, as was the degree of recovery. Follow-up over two years showed that children who had had mild or moderate poisoning slowly but steadily improved, some of them recovering normal function, though all had a residual generalized hyperreflexia. In some patients ataxia and motor weakness disappeared. Visual changes also improved, though less completely, and of 17 blind children, only five had recovered partial sight by the end of two years. Seven of the 18 children who suffered very severe poisoning were left physically and mentally incapacitated. The degree of clinical progress shown by these children was better than that shown by some other groups of patients, possibly because the poisoning was relatively acute and mercury consumption was stopped immediately after its effects had become obvious.

Adolescent↗
PubMed1978

Exchange transfusion treatment of methylmercury-poisoned children.

Three children, ages 6 months, 13 months and 10 years were treated by exchange transfusions following exposure to methylmercury in the Iraq outbreak in 1971-72. Two had severe signs of poisoning and the other was clinically normal but had a high blood mercury concentration. Exchange transfusion resulted in clearance of mercury not only from blood but also from other tissues. The average amount of mercury removed in a two hour exchange was estimated as 6% of the body burden as compared to 1% of the body burden removed by normal excretion processes in 24 hours. No dramatic improvement in the clinical condition of the two poisoned patients occurred. Some improvement in motor power and function was observed during follow-up visits to their houses.

Child↗
PubMed1976

Perinatal methylmercury poisoning in Iraq.

The signs and symptoms of methylmercury poisoning and the concentrations of mercury in samples of blood, hair, and milk are reported and compared in two infant-mother pairs exposed in the recent Iraq outbreak. In one pair, the infant was born prior to the exposure of the mother, and was exposed only from ingestion of methylmercury in mother's milk. In the other pair, the mother was exposed during pregnancy and did not breast feed the infant, who died 30 days after birth. Both mothers had some signs and symptoms of poisoning, but the infants did not. The infants had maximum estimated blood mercury levels between 500 and 1,000 ng/ml, well above the minimum toxic levels for adults. Hair and blood concentrations of mercury correlated closely, the average hair-blood ratio being about 250. Maternal milk averaged 8.6% of the simultaneous blood level, but the relationship was nonlinear at blood mercury levels below 50 ng/ml. Postnatal exposure by suckling led to substantial infant blood mercury concentration (over 600 ng/ml), and prenatal exposure resulted in blood mercury levels in the infant at birth higher than those in the mother, even after corrections for differences in hematocrit level.

Adult↗