Environmental Engineering Reference
In-Depth Information
In the period-specifi c analysis, limited to defects with the highest prevalence, we
found little evidence of changes in risk during the shut-down of the plant, since the OR
among “exposed” women was substantially similar to that computed for the operation
period (Table 2).
DISCUSSION
A limited number of epidemiologic studies investigated the risk of congenital anoma-
lies among populations directly exposed to the emissions of waste incinerators [5,
18-23]. Some studies did not find an increased prevalence of overall anomalies or of
specific groups of birth defects, while others detected excess risks for nervous system
anomalies [21], cardiovascular defects [21], facial cleft [19, 22], urinary defects [22],
and overall infant deaths due to congenital malformations [23]. However, method-
ological limitations considerably hamper the evaluation of results of most investiga-
tions: very few studies analyzed maternal residence during the first 3 months of gesta-
tion, or adjusted for maternal age and for socioeconomic status. Moreover, distance
of maternal residence (at time of delivery or abortion) from the plant was generally
considered in exposure assessment, without taking into consideration the characteris-
tics of the plant (chimney heights and widths, type and amount of combusted waste),
the amount of waste combusted and the meteorological factors, with the noticeable
exception of the study by Cordier et al. [22] who used an exposure index estimated
from a Gaussian plume model.
Overall, results of the present study did not suggest the occurrence of an excess
teratogenic risk in the vicinity of the incinerator plant, since prevalence increased only
in the medium-exposure area and such increase was statistically very unstable, nor
any evidence of reduction in risk during shut-down of the plant emerged. Moreover,
a more specifi c analysis for single categories of anomalies did not generally lead us
to identify excess risks for any disease group, though these results must be evaluated
with caution since most of the computed estimates were statistically unstable. In par-
ticular, urogenital anomalies such hypospadias, an abnormality suspected to be associ-
ated with parental exposure to environmental endocrine disrupting chemicals [24, 25],
did not increase in the exposed population. However, we found an excess prevalence
of chromosomal anomalies in middle exposure area, which is diffi cult to interpret
since there risk was not increased in the high exposure area, and no association was
found in the two epidemiologic studies which specifi cally examined this category of
birth defects [20, 22]. We therefore consider it useful to further monitor this fi nding in
the study area or in other comparable contexts.
Some degree of exposure misclassifi cation certainly occurred in the present study.
First, since chlorinated compounds are contaminants characterized by persistency in
the human body and in the environment, assessment of exposure based on residence
during gestation and not on long-term residential history or the occupational environ-
ment might have biased to some extent the actual exposure burden experienced by
the study subjects during the latest years. However, we checked in a random sample
of case and referent women (n = 46, 10% of the study population) their residences 3
years before date of delivery or abortion, in order to ascertain the extent of long-term
changes in exposure status. We found that 36 (78.3%) were then residing in the same
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