BackgroundLimited epidemiologic studies have examined the association between maternal low-level lead exposure [blood lead (PbB) < 10 μg/dL] and fetal growth.ObjectiveWe examined whether maternal low-level lead exposure is associated with decreased fetal growth.MethodsWe linked New York State Heavy Metals Registry records of women who had PbB measurements with birth certificates to identify 43,288 mother–infant pairs in upstate New York in a retrospective cohort study from 2003 through 2005. We used multiple linear regression with fractional polynomials and logistic regression to relate birth weight, preterm delivery, and small for gestational age to PbB levels, adjusting for potential confounders. We used a closed-test procedure to identify the best fractional polynomials for PbB among 44 combinations.ResultsWe found a statistically significant association between PbB (square root transformed) and birth weight. Relative to 0 μg/dL, PbBs of 5 and 10 μg/dL were associated with an average of 61-g and 87-g decrease in birth weight, respectively. The adjusted odds ratio for PbBs between 3.1 and 9.9 μg/dL (highest quartile) was 1.04 [95% confidence interval (CI), 0.89–1.22] for preterm delivery and 1.07 (95% CI, 0.93–1.23) for small for gestational age, relative to PbBs ≤ 1 μg/dL (lowest quartile). No clear dose–response trends were evident when all of the quartiles were assessed.ConclusionsLow-level PbB was associated with a small risk of decreased birth weight with a supralinear dose–response relationship, but was not related to preterm birth or small for gestational age. The results have important implications regarding maternal PbB.

A significant positive association was observed with height one year before diagnosis (P-value for trend = 0.02). No significant associations were observed between osteosarcoma and weight of body mass index one year before diagnosis, birth length, birthweight, gestational age, having reached puberty, having begun growth spurt, age at puberty, age growth spurt began, medical x-rays, antenatal exposures, family history of cancer, birth defects, or parental occupation.

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OBJECTIVES. This study tests the hypothesis that fluoride exposure in a nonoccupational setting is a risk factor for childhood osteosarcoma. METHODS. A population-based case-control study was conducted among residents of New York State, excluding New York City. Case subjects (n = 130) were diagnosed with osteosarcoma between 1978 and 1988, at age 24 years or younger. Control subjects were matched to case subjects on year of birth and sex. Exposure information was obtained by a telephone interview with the subject, parent, or both. RESULTS. Based on the parents' responses, total lifetime fluoride exposure was not significantly associated with osteosarcoma among all subjects combined or among females. However, a significant protective trend was observed among males. Protective trends were observed for fluoridated toothpaste, fluoride tablets, and dental fluoride treatments among all subjects and among males. Based on the subjects' responses, no significant associations between fluoride exposure and osteosarcoma were observed. CONCLUSIONS. Fluoride exposure does not increase the risk of osteosarcoma and may be protective in males. The protective effect may not be directly due to fluoride exposure but to other factors associated with good dental hygiene. There is also biologic plausibility for a protective effect.