Brenda Eskenazi

Background: Farmworkers and their families are at risk for pesticide exposure, however, little is known about behaviors that increase their risk. We determined the frequency of risky behaviors among pregnant farmworkers and characterized those at greatest risk.Methods: Participants included 153 pregnant farmworkers and 248 pregnant non‐farmworkers who resided with farmworkers from the CHAMACOS (Center for the Health Assessment of Mothers and Children of Salinas) study. We examined risky behaviors relating to handwashing, bathing, protective clothing, house cleaning, laundering of work clothes, wearing of work clothes and shoes into the home, and eating produce from the fields.Results: Between 25 and 60% of women demonstrated risky behavior on each item. Practices of households with pregnant farmworkers and non‐farmworkers did not differ. Women who lived in the United States longer, and in crowded households demonstrated the most risky behavior overall.Conclusions: Pregnant farmworkers and those living with farmworkers need to be educated to reduce potential take‐home pesticide exposure. Am. J. Ind. Med. 45:491–499, 2004.

Environmental Health Perspectives is an Open Access journal published by the National Institute of Environmental Health Sciences. Environmental Health Perspectives is an Open Access journal published by the National Institute of Environmental Health Sciences.

BACKGROUND: Although the effect of maternal age on fertility is well known, it is unclear whether paternal age also affects fertility. This cross‐sectional study sought to characterize the association between age and semen quality, a well‐known proxy of fertility status. METHODS: A convenience sample of 97 non‐smoking men (aged 22–80 years) without known fertility problems was recruited from a national government laboratory. The men provided semen samples and information relating to lifestyle, diet, medical and occupational details. Semen volume (ml), sperm concentration (×10⁶/ml), total sperm count (×10⁶), motility (%), progressive motility (%) and total progressively motile sperm count (×10⁶) were measured. RESULTS: After adjusting for covariates, semen volume decreased by 0.03 ml per year of age (95% CI: –0.05, –0.01); motility decreased by 0.7% per year (95% CI: –0.92, –0.43); progressive motility decreased by 3.1% per year (95% CI: –4.5, –1.6); and total progressively motile sperm count decreased by 4.7% per year (95% CI: –7.2, –2.2). There was a suggested decrease in sperm concentration and count. The proportion of men with abnormal volume, concentration and motility was significantly increased across the age decades. CONCLUSIONS: In a convenience sample of healthy men from a non‐clinical setting, semen volume and sperm motility decreased continuously between 22–80 years of age, with no evidence of a threshold.

BACKGROUND: It is unclear whether frequency of sperm aneuploidy is associated with risk of fathering children with trisomy. METHODS: We recruited 36 families with a boy with Klinefelter syndrome (KS), interviewed the fathers about their exposures and medical history, received a semen sample from each father, and collected blood samples from the mother, father and child. We applied a multicolour fluorescent in-situ hybridization assay to compare the frequencies of sperm carrying XY aneuploidy and disomies X, Y and 21 in fathers of maternally and paternally inherited KS cases. RESULTS: Inheritance of the extra X chromosome was paternal in 10 and maternal in 26 families. Fathers of paternal KS cases produced higher frequencies of XY sperm (P = 0.02) than fathers of maternal KS cases. After controlling for age, the major confounding variable, the difference between the two groups was no longer significant (P ≤ 0.2). Also, there were no significant differences between the parental origin groups for disomy X, Y or 21. CONCLUSIONS: Men who fathered a child with a Klinefelter syndrome produced higher frequencies of XY sperm aneuploidy, which is explained, in part, by both paternal age and parent of origin.

Pre-eclampsia is characterized by abnormal implantation of the trophoblast in the placenta and poor placental perfusion, followed by sustained hypertension and proteinuria. While the disease has been recognized for centuries, the aetiology of pre-eclampsia is unknown and is likely multifactorial. Clues about the aetiology of pre-eclampsia might be derived from the risk factors that have been identified. However, to date, the only well-accepted risk factor for pre-eclampsia is primiparity. Recently, it has been suggested that primipaternity rather than primiparity is the relevant risk factor.¹ That is, that not only are primiparas at high risk but so are multiparas having a first child with a new father.^{2– 6}