C O'Leary1, P Jacoby, H D'Antoine, A Bartu, C Bower. 1. Centre for Population Health Research, Curtin Health Information Research Institute, Curtin University, Perth, WA, Australia. colleen.oleary@curtin.edu.au
Abstract
OBJECTIVE: To investigate the association between heavy prenatal alcohol exposure and stillbirth. DESIGN: Data linkage cohort study. SETTING: Western Australia (WA). POPULATION: The exposed cohort included mothers with an alcohol-related diagnosis (International Classification of Diseases, ninth/tenth revisions) recorded in health data sets and all their offspring born in WA (1983-2007). Mothers without an alcohol-related diagnosis and their offspring comprised the comparison cohort. METHODS: Exposed and comparison mothers were identified through the WA Data Linkage System. Odds ratios for stillbirth at 20+ weeks of gestation were estimated by logistic regression, stratified by Aboriginal status. MAIN OUTCOME MEASURES: The proportion of stillbirths at 20+ weeks of gestation is presented per 1000 births, as well as adjusted odds ratios (aOR) and 95% confidence intervals (95% CI), and population-attributable fractions. RESULTS: Increased odds of stillbirth were observed for mothers with an alcohol-related diagnosis at any stage of their life for both non-Aboriginal (aOR 1.36; 95% CI 1.05-1.76) and Aboriginal (aOR 1.33; 95% CI 1.08-1.64) births. When an alcohol diagnosis was recorded during pregnancy, increased odds were observed for non-Aboriginal births (aOR 2.24; 95% CI 1.09-4.60), with the highest odds of Aboriginal stillbirth occurring when an alcohol diagnosis was recorded within 1 year postpregnancy (aOR 2.88; 95% CI 1.75-4.73). The population-attributable fractions indicate that 0.8% of non-Aboriginal and 7.9% of Aboriginal stillbirths are the result of heavy alcohol consumption. CONCLUSIONS: Prevention of heavy maternal alcohol use has the potential to reduce stillbirths. The lack of an association between exposure during pregnancy and Aboriginal stillbirth in this study needs further investigation.
OBJECTIVE: To investigate the association between heavy prenatal alcohol exposure and stillbirth. DESIGN: Data linkage cohort study. SETTING: Western Australia (WA). POPULATION: The exposed cohort included mothers with an alcohol-related diagnosis (International Classification of Diseases, ninth/tenth revisions) recorded in health data sets and all their offspring born in WA (1983-2007). Mothers without an alcohol-related diagnosis and their offspring comprised the comparison cohort. METHODS: Exposed and comparison mothers were identified through the WA Data Linkage System. Odds ratios for stillbirth at 20+ weeks of gestation were estimated by logistic regression, stratified by Aboriginal status. MAIN OUTCOME MEASURES: The proportion of stillbirths at 20+ weeks of gestation is presented per 1000 births, as well as adjusted odds ratios (aOR) and 95% confidence intervals (95% CI), and population-attributable fractions. RESULTS: Increased odds of stillbirth were observed for mothers with an alcohol-related diagnosis at any stage of their life for both non-Aboriginal (aOR 1.36; 95% CI 1.05-1.76) and Aboriginal (aOR 1.33; 95% CI 1.08-1.64) births. When an alcohol diagnosis was recorded during pregnancy, increased odds were observed for non-Aboriginal births (aOR 2.24; 95% CI 1.09-4.60), with the highest odds of Aboriginal stillbirth occurring when an alcohol diagnosis was recorded within 1 year postpregnancy (aOR 2.88; 95% CI 1.75-4.73). The population-attributable fractions indicate that 0.8% of non-Aboriginal and 7.9% of Aboriginal stillbirths are the result of heavy alcohol consumption. CONCLUSIONS: Prevention of heavy maternal alcohol use has the potential to reduce stillbirths. The lack of an association between exposure during pregnancy and Aboriginal stillbirth in this study needs further investigation.
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