[Show abstract][Hide abstract] ABSTRACT: A previous study suggested a younger age at menarche (AAM) among daughters of heavy prenatal smokers, especially among non-Whites. The present study was designed to evaluate that association in another population and to examine other factors that may be related to AAM. We analysed data from the Collaborative Perinatal Project, a nationwide longitudinal study of pregnant women and their children conducted in 1959–66. At three sites, with a predominance of Black participants (80%), AAM was ascertained in the offspring when they were young adults. We included data on 1556 daughters who had a mean AAM of 12.7 years (standard deviation 1.8). Amount smoked by the mothers was obtained from a baseline interview and subsequent prenatal visits. Regression models were run including maternal smoking and other covariates, for only the prenatal period, as well as in models with some childhood characteristics.
In the prenatal factor model, younger mean AAM in daughters was found with maternal characteristics of earlier AAM, being married, and of lower parity. Examining childhood variables, earlier AAM was found among girls with few or no siblings or with higher socio-economic status. Unlike our previous findings, mean AAM was later in daughters of heavy smokers (20+ cigarettes/day), with a delay of 0.31 years [95% confidence interval (CI) 0.008, 0.61], or about 3.7 months in the prenatal model, and 0.34 years [95% CI −0.02, 0.66] in the model with childhood variables included. The pattern was consistent by race. A number of prenatal and childhood factors related to AAM were identified that should be considered when examining exogenous exposures in relation to pubertal onset.
[Show abstract][Hide abstract] ABSTRACT: To explore possible associations between autism spectrum disorders (ASD) and environmental exposures, we linked the California autism surveillance system to estimated hazardous air pollutant (HAP) concentrations compiled by the U.S. Environmental Protection Agency.
Subjects included 284 children with ASD and 657 controls, born in 1994 in the San Francisco Bay area. We assigned exposure level by census tract of birth residence for 19 chemicals we identified as potential neurotoxicants, developmental toxicants, and/or endocrine disruptors from the 1996 HAPs database. Because concentrations of many of these were highly correlated, we combined the chemicals into mechanistic and structural groups, calculating summary index scores. We calculated ASD risk in the upper quartiles of these group scores or individual chemical concentrations compared with below the median, adjusting for demographic factors.
The adjusted odds ratios (AORs) were elevated by 50% in the top quartile of chlorinated solvents and heavy metals [95% confidence intervals (CIs) , 1.1-2.1], but not for aromatic solvents. Adjusting for these three groups simultaneously led to decreased risks for the solvents and increased risk for metals (AORs for metals: fourth quartile = 1.7 ; 95% CI, 1.0-3.0 ; third quartile = 1.95 ; 95% CI, 1.2-3.1) . The individual compounds that contributed most to these associations included mercury, cadmium, nickel, trichloroethylene, and vinyl chloride.
Our results suggest a potential association between autism and estimated metal concentrations, and possibly solvents, in ambient air around the birth residence, requiring confirmation and more refined exposure assessment in future studies.
Environmental Health Perspectives 10/2006; 114(9):1438-44. DOI:10.1289/ehp.9120 · 7.98 Impact Factor