CONTAMINATION OF HOUSES BY WORKERS OCCUPATIONALLY EXPOSED IN A LEAD-ZINC-COPPER MINE AND IMPACT ON BLOOD LEAD CONCENTRATIONS IN THE FAMILIES

Citation
M. Chiaradia et al., CONTAMINATION OF HOUSES BY WORKERS OCCUPATIONALLY EXPOSED IN A LEAD-ZINC-COPPER MINE AND IMPACT ON BLOOD LEAD CONCENTRATIONS IN THE FAMILIES, Occupational and environmental medicine, 54(2), 1997, pp. 117-124
Citations number
23
Categorie Soggetti
Public, Environmental & Occupation Heath
ISSN journal
13510711
Volume
54
Issue
2
Year of publication
1997
Pages
117 - 124
Database
ISI
SICI code
1351-0711(1997)54:2<117:COHBWO>2.0.ZU;2-4
Abstract
Objective-To evaluate the pathway of leaded dust from a lead-zinc-copp er mine to houses of employees, and the impact on blood lead concentra tions (PbB) of children. Methods-High precision lead isotope and lead concentration data were obtained on venous blood and environmental sam ples (vacuum cleaner dust, interior dustfall accumulation, water, pain t) for eight children of six employees (and the employees) from a lead -zinc-copper mine. These data were compared with results for 11 childr en from occupationally unexposed control families living in the same c ity. Results-The median (range) concentrations of lead in vacuum clean er dust was 470 (21-1300) ppm. In the houses of the mine employees, va cuum cleaner dust contained varying higher proportions of mine lead th an did airborne particulate matter measured as dustfall accumulated ov er a three month period. The median (range) concentrations of lead in soil were 30 (5-407) ppm and these showed no evidence of any mine lead . Lead in blood of the mine employees varied from 7 to 25 mu g/dl and was generally dominated by mine lead (> 60%). The mean (SD) PbB in the children of the mine employees was 5 . 7 (1 . 7) mu g/dl compared wit h 4 . 1 (1 . 4) mu g/dl for the control children (P = 0 . 02). The PbB of all children was always < 10 mu g/dl, the Australian National Heal th and Medical Research Council goal for all Australians. Some of the control children had higher PbB than the children of mine employees, p robably from exposure to leaded paint as six of the eight houses of th e control children were > 50 years old. In five of the eight children of mine employees > 20% of PbB was from the lead mine. However, in the other three cases of children of mine employees, their PbB was from s ources other than mine lead (paint, petrol, background sources). Concl usions-Houses of employees from a lead mine can be contaminated by min e lead even if they are not situated in the same place as the mine. De lineation of the mine to house pathway indicates that lead is probably transported into the houses on the clothes, shoes, hair, skin, and in some cases, motor vehicles of the workers. In one case, dust shaken f rom clothes of a mine employee contained 3000 ppm lead which was 100% mine lead. The variable contamination of the houses was not expected g iven the precautions taken by mine employees to minimise transportatio n of lead into their houses. Although five out of the eight children o f mine employees had > 20% mine lead in their blood, in no case did th e PbB of a child exceed the Australian National Health and Medical Res earch Council goal of 10 mu g/dl. In fact, some children in the contro l families had higher PbB than children of mine employees. In two case s, this was attributed to a pica habit for paint. The PbB in the child ren of mine employees and controls was independent of the source of le ad. The low PbB in the children of mine employees may reflect the rela tively low solubility (bioavailability) of the mine dust in 0 . 1 M hy drochloric acid (< 40%), behaviour-for example, limited mouthing activ ity-or diet.