Environmental exposure of the pediatric age groups in Cairo City and its suburbs to cadmium pollution
Introduction
Cadmium (Cd) is one of the metals considered to be potentially dangerous on a global level. It is a known human carcinogen and one of the components of tobacco, which, together with water and food contamination, represent the main sources of non-occupational exposure in the general population (Elinder, 1985, Willers et al., 1992, Jarup et al., 1998). Cd has an extremely long biological half-life of more than 15 years in humans (Alcock, 1996, Jin et al., 1998, Viaene et al., 1999). Only a very small fraction of Cd is excreted and the total body content increases with age (Bender and Bender, 1997).
It has been known for decades that Cd exposure can cause a variety of adverse health effects, among which kidney dysfunction, lung diseases and disturbed calcium metabolism and bone defects are the most prominent (Jin et al., 1998). Following long-term exposure, the kidney is the critical organ. The most frequent long-term consequence is proteinuria, and it may precede a slowly progressive and irreversible renal tubular dysfunction (Iwata et al., 1993). It was postulated that cadmium pollution in many industrialized areas could accelerate age-related decline of renal function in populations without occupational exposure (Grandjean, 1998). Cd workers frequently suffer from varying degrees of obstructive lung disease (Mc Callum, 1987). Itai Itai disease is the name that was given to an outbreak of osteomalacia reported in multiparous women in Japan. It was first noted in an area where the crops became contaminated with Cd due to irrigation by water that was drained through an old zinc mine (Mc Callum, 1987). Cd has since been considered a risk factor for osteoporosis (Jarup et al., 1998) and was found to interfere with vitamin D3 hydroxylation in the kidney (Chalkley et al., 1998). Some other reported health hazards from Cd include arterial hypertensive disease (Kopp, 1986, Luoma, 1998), polyneuropathy (Viaene et al., 1999), impairment of thyroid functions in children (Osius et al., 1999) and suppression of immediate hypersensitivity response and immunoglobulin G level in school children (Ritz et al., 1998). Moreover, transplacental transport was frequently reported and a placental barrier was suggested, as the cord blood levels ranged from 40 to 70% of the maternal level in most studies (Huel et al., 1981, Korpela et al., 1986, Krachler et al., 1999, Mokhtar et al., 1999, Odland et al., 1999). Mokhtar et al. (1999) noticed a negative correlation between umbilical cord serum Cd levels and the APGAR scores of 100 Egyptian neonates.
With this as a background, and knowing that children can be at risk from environmental exposure to toxins at a lower level than is acceptable for adults (Price et al., 1999), we were stimulated to study the Cd status of a sample of Cairene subjects in the pediatric age group to uncover the risk and raise the public awareness towards its prevention.
Section snippets
Subjects
This cross-sectional study comprised 405 subjects, 0–18 years old, living in Cairo City and its suburbs. They were enrolled from the outpatient clinic and casualty of the Children's Hospital of Ain Shams University in Cairo after exclusion of chronic or debilitating diseases. All subjects belonged to the low and middle socio-economic classes in Egypt that attend the free-of-charge medical facilities of the Ain Shams University Hospitals, Cairo. They were enrolled while presenting for feeding
Cadmium estimation:
A venous blood sample (2–3 ml) was collected from every subject by venipuncture. The serum was separated by centrifugation at 1800 rev./min for 10 min after 2 h of incubation at 25°C and then collected in clean, metal-free tubes. Hemolyzed samples were discarded. The serum samples were stored at −20°C until assayed for Cd in the same lab setting. Breast milk samples were expressed by all mothers of the breast fed infants (n=30) in metal-free containers and were stored at −20°C until assayed for
Results
Serum Cd levels ranged between 0.15 and 2.4 μg/l in the neonates, with a geometric mean (G.S.D.) of 0.92 (1.9) μg/l. This level was significantly lower than that of the infants, being 1.33 (1.5) μg/l, (range 0.55–3.21 μg/l, P<0.01. The latter value was statistically comparable to the corresponding geometric means of the remaining groups, being 1.11 (1.6) μg/l (range 0.49–3.81 μg/l) in the 2–6-year olds, 1.34 (1.6) μg/l (range 0.63–3.9 μg/l) in the 6–12-year old children and 1.24 (1.5) μg/l
Discussion
Cadmium was detectable in the 405 serum samples tested, ranging from 0.15 up to 3.9 μg/l. The neonates expressed the lowest geometric mean, being 0.92 μg/l. Beyond the neonatal period the levels rose significantly, to 1.33 μg/l in infants, 1.11 μg/l in preschool children, 1.34 μg/l in the 6–12-year-old children and 1.24 μg/l in adolescents. The differences between the last four groups were insignificant. A review of the literature indicated that Cd is present in human infants in very low
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