The best estimate isthat after short-term exposure to mercury vapour, thefirst phase of elimination from blood has a half-time ofapproximately 2-4 days and accounts for about 90% of themercury.
This relationship (section 5.1)indicates that ongoing long-term exposure to elementalmercury vapour, leading to a mercury absorption of5-10 µg/day, will result in a mercury excretion in urineof about 5 µg/litre and average mercury concentrationsin the occipital lobe cortex and kidney of approximately10 µg/kg and 500 µg/kg, respectively.
To evaluate the relation between early exposure to lead and each of the continuously distributed outcome variables, subjects were classified according to dentin lead-level quartiles, and mean scores, adjusted for covariates, were computed. Ordinary least-squares linear regression, with the mean or log-mean dentin lead level as the main effect, was used to estimate the significance of the relation. Outcomes that were significantly associated with lead exposure in these bivariate analyses were further evaluated by multiple regression analysis. Ten covariates were included in the model. They were the mother's age at the time of the subject's birth, the mother's educational level, the mother's IQ, family size, socioeconomic status (a two-factor Hollingshead index), sex, age at the time of testing, birth order, alcohol use, and whether the subject and the mother left the hospital together after the subject's birth. The lead measure (the mean or the log of the mean) that produced the best-fitted model (highest R2) is reported. Five of these covariates were employed in the first study of these subjects and shown to be influential. Five others (sex, age at testing, prolonged hospitalization as a neonate, birth order, and current alcohol use) were added to the model on the basis of prior knowledge of their effects on psychometric function. Logistic-regression analysis was used to model the association of lead level and two outcomes treated categorically (failure to graduate from high school and reading disability). In this analysis, we controlled for the covariates listed above. Two indicator variables were used to represent the three exposure groups. Odds ratios and 95 percent confidence intervals, adjusted for covariates, were computed for the high-lead-level group, with the lowlead-level group used as the reference group.
A broad community requires globally consistent estimates of long-term PM2.5 exposure and changes over time. For example, this information is used for Global Burden of Disease assessments (; ; ), for environmental performance indicators (), and for epidemiologic studies of air pollution health effects at global (; ) and regional (; ; ) scales. Satellite retrievals offer the most globally complete observationally based data source of this information, but improvements to these estimates are needed to reduce uncertainties.
Long-term time-weighted occupational exposure to an aver-age air mercury concentration of 50 µg/m3 was consideredto be associated, on a group basis, with blood mercurylevels of approximately 35 µg/litre, and with urinaryconcentrations of 150 µg/litre.
Thetype of chemical exposure (whether to elemental mercury orto mercuric mercury salts) is an important determinant forthe toxic effect and to differences in distribution.
N Bourjeily, J.B Suszkiw. . (1997) Developmental cholinotoxicity of lead: loss of septal cholinergic neurons and long-term changes in cholinergic innervation of the hippocampus in perinatally lead-exposed rats. 771, 319-328.
In suscep-tible strains of mice, especially those mice carrying theH-2s haplotype, long-term exposure to mercuric chlorideinduces extremely high titres of antinucleolar auto-anti-bodies (Robinson et al., 1986; Mirtscheva et al., 1987).
Li Sui, Di-Yun Ruan, Shao-Yu Ge, Xiao-Mei Meng. . (2000) Two components of long-term depression are impaired by chronic lead exposure in area CA1 and dentate gyrus of rat hippocampus in vitro. 22, 741-749.
After short-term exposure of experimental animals tomethylmercury the kidneys usually contain the highestfraction of Hg++ in relation to total mercury, while therelative concentration in the brain is low (WHO, 1976).
Bumin Dundar, Faruk Öktem, Meltem Koyuncu Arslan, Namık Delibas, Bahattin Baykal, Çağatay Arslan, Mustafa Gultepe, Inci Ergurhan Ilhan. . (2006) The effect of long-term low-dose lead exposure on thyroid function in adolescents. 101, 140-145.
Mercury has beenfound intracellularly in nerve cells after exposure tomercury vapour (Cassano et al., 1966) and also after pro-longed exposure to mercuric chloride in the rat (Moller-Madsen & Danscher, 1986).
Exposure from dental amalgam220.127.116.11 Human studies The release of mercury vapour from dental amalgamfillings has been known for a very long time (Stock,1939).
Amelia K. Searle, Peter A. Baghurst, Miranda van Hooff, Michael G. Sawyer, Malcolm R. Sim, Cherrie Galletly, Levina S. Clark, Alexander C. McFarlane. . (2014) Tracing the long-term legacy of childhood lead exposure: A review of three decades of the Port Pirie Cohort study. .
Occu-pational exposure to metallic mercury has long beenassociated with the development of proteinuria, both inworkers with other evidence of mercury poisoning and inthose without such evidence.