Abstract
OBJECTIVES: to evaluate risk factors involving environmental and occupational parental exposures associated with occurrence of orofacial clefts in a group of Brazilian children. METHODS: a secondary base case-control study was conducted with 274 cases of cleft lip with or without cleft palate (CL±P) and cleft palate only, with 548 controls (1:2). The authors analyzed residential proximity to industrial areas, exposure to commercial insecticides, agricultural pesticides, and vector control spraying, as well as various occupational exposures. The results were obtained by conditional regression analysis. RESULTS: proximity to industrial installations as a risk factor (OR = 3,32; 95%CI: 2,18-5,05) for all orofacial clefts, as well as the combined use of household insecticides and urban vector control pesticide spraying (OR = 5,73; 95%CI: 2,51-11,28). A group of maternal occupations heavily associated with orofacial clefts was domestic services (OR = 2,89; 95%CI: 1,76-4,86). CONCLUSIONS: solvents are frequently associated with CL ± P and that they are contained in numerous industrial products and household cleaning products, the results pertaining to occupational exposure become plausible. Other associations such as the routine use of domestic insecticides require further specific research for confirmation of the hypothesis.
Highlights
The association between congenital malformations and maternal occupational exposure has been described in numerous epidemiological studies
Household exposure to insecticide use combined with pesticide spraying by Ministry of Health vector control agents showed increased risk both for the pre-gestational period and first trimester of the index pregnancy
The active ingredients most commonly identified among the commercial insecticides were pyrethroids and pyrethrins, with a grade II toxicological classification
Summary
The association between congenital malformations and maternal occupational exposure has been described in numerous epidemiological studies. It is felt that potentially harmful exposures can affect parental germ cells before conception or embryonic somatic cells after conception. In both situations cell death can be induced, as well as cellular dysfunctions leading to congenital malformations.[3] Such observations have gained greater importance as the proportion of childbearing-age women in both the formal and informal labor markets has increased progressively in various countries, including Brazil.[4]. Few epidemiological studies have been conducted to measure the consequences, for example, of a potential increase in the distribution of congenital malformations in the offspring of individuals exposed to specific teratogenic agents. The two main difficulties are the measurement of these multiple sources and the use of prevalent malformations for outcome analysis, which can be interpreted as resulting from the effect of survival within a cohort of malformed offspring.[6]
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