Personal injury recovery cost of pedestrian–vehicle collisions in New South Wales,Australia

Background: There is a need for routine estimates of injury recovery costs from pedestrian collisions using hospital separation records for economic evaluations.

Objective: To estimate the cost of injury recovery following pedestrian–vehicle collisions using the personal injury recover cost (PIRC) equation using key demographic and injury characteristics.

Method: An estimation of the costs of on-road pedestrian–vehicle collisions involving individuals who were injured and hospitalized in New South Wales (NSW), Australia, from 2002 to 2011 using the PIRC equation. The PIRC estimates individual injury recovery costs and does not include costs associated with property damage, vehicle repair, or rescue services. Individual recovery costs associated with severe traumatic brain injury (TBI) were estimated. The injured individual's mean, median, and total injury recovery costs are described for key demographic, injury, and crash characteristics.

Results: There were 9,781 pedestrians who were injured, costing an estimated total of $2.4 billion in personal injury recovery costs, an annual cost of $243 million. Males had a total injury recovery cost 1.7 times higher than females. The median injury recovery cost decreased with increasing age. TBI ($248,491) and spinal cord and vertebral column injuries ($264,103) had the highest median injury recovery costs for the body region of the most severe injury. TBI accounted for 22.6% of the total injury recovery costs for the most severe injury sustained. Just over one third of pedestrians sustained 4 or more injuries, with a median cost of $243,992, which was 1.6 times higher than the cost for a pedestrian who sustained a single injury ($153,682).

Conclusions: Personal injury recovery costs following pedestrian–vehicle collisions where a pedestrian is injured are substantial in NSW. The PIRC equation enables the economic cost burden of road traffic injury to be calculated using hospital separation data. The PIRC enables comprehensive personal injury recovery costs to be estimated and would aid in economic evaluations of preventive strategies in road safety.     

Managing mercury in the great lakes: an analytical review of abatement policies

Mercury, a toxic metal known to have several deleterious affects on human health, has been one of the principal contaminants of concern in the Great Lakes basin. There are numerous anthropogenic sources of mercury to the Great Lakes area. Combustion of coal, smelting of non ferrous metals, and incineration of municipal and medical waste are major sources of mercury emissions in the region. In addition to North American anthropogenic emissions, global atmospheric emissions also significantly contribute to the deposition of mercury in the Great Lakes basin. Both the USA and Canada have agreed to reduce human exposure to mercury in the Great Lakes basin and have significantly curtailed mercury load to this region through individual and joint efforts. However, many important mercury sources, such as coal-fired power plants, still exist in the vicinity of the Great Lakes. More serious actions to drastically reduce mercury sources by employing alternative energy sources, restricting mercury trade and banning various mercury containing consumer products, such as dental amalgam are as essential as cleaning up the historical deposits of mercury in the basin. A strong political will and mass momentum are crucial for efficient mercury management. International cooperation is equally important. In the present paper, we have analyzed existing policies in respective jurisdictions to reduce mercury concentration in the Great Lakes environment. A brief review of the sources, occurrence in the Great Lakes, and the health effects of mercury is also included.     

Apolipoproteins in human fetal blood and amniotic fluid in mid-trimester pregnancy

To examine the potential for prenatal diagnosis of genetic lipoprotein metabolic defects (e.g. abetalipoproteinemia, Tangier disease) we determined the normal concentrations of apolipoproteins (apo) A-I, A-II, B, and E in mid-trimester amniotic fluid and fetal plasma. The concentrations of apo A-I and apo A-II in amniotic fluid were 1−2 per cent of the respective levels in the mother's plasma, whereas apo B and apo E were undetectable in amniotic fluid. In contrast to amniotic fluid, all four apolipoproteins were detectable in fetal plasma, and the levels of apo A-I, apo B and apo E were in the range observed in the mothers: 160·2 ± 103·1, 59·8 ± 35·7 and 5·7 ± 3·5 mg/dl respectively (mean ± SD, n=13). The fetal plasma level of apo A-II (28·3 ± 12·4 mg/dl) was two-thirds that observed in the mother's plasma. The normal levels of these apolipoproteins in fetal plasma are well above the sensitivity of the methods, and their quantification requires only 10−20 μl of fetal plasma. Determination of apolipoproteins in fetal blood obtained by fetoscopy thus may provide a method for the prenatal diagnosis of congenital apolipoprotein deficiences.     

Ontogeny of fetal liver glucose-6-phosphatase activity

A reliable and sensitive microassay for the measurement of liver glucose-6-phosphatase is described. Human fetal liver was assayed for glucose-6-phosphatase activity from 7.5 to 24 weeks of gestation and was found to have a mean activity of 2.11 nmol per min per mg of protein. This was approximately 30 per cent of the postnatal controls assayed by the same method, but there was no evidence of a change in activity during the gestational period examined. If fetal liver tissue can be reliably obtained, it may be possible to determine a deficiency of glucose-6-phosphatase in fetuses who are at risk.