BACKGROUND: Hexachlorobenzene (HCB) is a ubiquitous environmental contaminant that, even at low doses, causes destruction of ovarian primordial germ cells in experimental studies. However, its potential for reproductive toxicity in humans exposed to background levels has not been fully evaluated. Here we examined the association between maternal levels of HCB and their infants' birth weight. METHODS: HCB was measured in milk samples from a subset of women in the Norwegian Human Milk Study (HUMIS), 2003-2006; 300 subjects were randomly chosen from the cohort and 26 from all small for gestational age (SGA) children. Additional information was obtained through questionnaires and the Medical Birth Registry. RESULTS: Overall, HCB was associated with birth weight (adjusted b = -90 g per 8 microg/kg milk fat, 95% CI-275 to 8) and with SGA (odds ratio 1.8, 95% CI 0.9-3.7 per 8 microg/kg milk fat (difference between the 10th and the 90th percentile)). After stratification, however, the association was present only among smokers. For birth weight for past or current smokers: b = -282, CI -467 to -98; for never smokers: b = 0.5, CI -149 to 150, p-value for interaction: 0.01. Similar results were observed for head circumference, crown-heel length, and SGA. CONCLUSIONS: We saw a moderate association between HCB and markers of impaired fetal growth among past and current smokers. This finding may be non-causal and due to underlying genetic variants tied to both growth and breakdown of HCB or to confounding by unmeasured toxicants that coexist in exposure sources. It may, however, also result from HCB exposure.
BACKGROUND:Hexachlorobenzene (HCB) is a ubiquitous environmental contaminant that, even at low doses, causes destruction of ovarian primordial germ cells in experimental studies. However, its potential for reproductive toxicity in humans exposed to background levels has not been fully evaluated. Here we examined the association between maternal levels of HCB and their infants' birth weight. METHODS:HCB was measured in milk samples from a subset of women in the Norwegian Human Milk Study (HUMIS), 2003-2006; 300 subjects were randomly chosen from the cohort and 26 from all small for gestational age (SGA) children. Additional information was obtained through questionnaires and the Medical Birth Registry. RESULTS: Overall, HCB was associated with birth weight (adjusted b = -90 g per 8 microg/kg milk fat, 95% CI-275 to 8) and with SGA (odds ratio 1.8, 95% CI 0.9-3.7 per 8 microg/kg milk fat (difference between the 10th and the 90th percentile)). After stratification, however, the association was present only among smokers. For birth weight for past or current smokers: b = -282, CI -467 to -98; for never smokers: b = 0.5, CI -149 to 150, p-value for interaction: 0.01. Similar results were observed for head circumference, crown-heel length, and SGA. CONCLUSIONS: We saw a moderate association between HCB and markers of impaired fetal growth among past and current smokers. This finding may be non-causal and due to underlying genetic variants tied to both growth and breakdown of HCB or to confounding by unmeasured toxicants that coexist in exposure sources. It may, however, also result from HCB exposure.
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